PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
32571380-8	2020	LIN28 rs7759938 genotypes TC + CC were higher in resolvers and controls than patients (P = 0.015).	Technetium	26-30	lin-28 homolog A	Homo sapiens	0-5
33516780-12	2021	Mechanistically, LINC0145 was shown to depend on LIN28A and LIN28B, facilitated epithelial-mesenchymal transition (EMT) through activating the TGF-beta/Smad signaling pathway, which subsequently aggravated BLCa progression.	linc0145	17-25	lin-28 homolog A	Homo sapiens	49-55
33742080-4	2021	We show here, using a structural and cellular approach, a mixing of Lin28 with YB-1 (YBX1) in the presence of mRNA owing to their cold-shock domain, a conserved beta-barrel structure that binds to ssRNA cooperatively.	ssrna	197-202	lin-28 homolog A	Homo sapiens	68-73
33412215-9	2021	SIGNIFICANCE: These results suggested that metformin modulated HG-induced endothelial ROS via the AMPKalpha/Lin-28/OGG1 pathway.	Metformin	43-52	lin-28 homolog A	Homo sapiens	108-114
33249080-3	2021	Herein, we studied the synergistic anti-tumor effect of a LIN28 inhibitor C1632 and hypoglycemic medication metformin in OSCC.	c1632	74-79	lin-28 homolog A	Homo sapiens	58-63
33249080-10	2021	Results showed that LIN28 and HMGA2 expression decreased significantly in SCC9 and CAL27 cells under 240 muM C1632 treatment for 72 h. These effects were synergized under combined treatment for 24 h. Cell proliferation ability and migration ability of both cell lines decreased significantly under respective and combined treatment.	c1632	109-114	lin-28 homolog A	Homo sapiens	20-25
32333719-3	2020	Here, we show that LIN28A is SUMOylated in vivo and in vitro at K15, which is increased by hypoxia but reduced by chemotherapy drugs such as Cisplatin and Paclitaxel.	Cisplatin	141-150	lin-28 homolog A	Homo sapiens	19-25
32333719-3	2020	Here, we show that LIN28A is SUMOylated in vivo and in vitro at K15, which is increased by hypoxia but reduced by chemotherapy drugs such as Cisplatin and Paclitaxel.	Paclitaxel	155-165	lin-28 homolog A	Homo sapiens	19-25
32560271-7	2020	Simultaneously with the increase of let-7 miRNAs in CAIX-suppressed cells, LIN28 protein levels decreased, along with downstream metabolic pathways: pyruvate dehydrogenase kinase 1 (PDK1) and phosphorylation of its substrate, pyruvate dehydrogenase (PDH) at Ser-232, causing attenuation of glycolysis.	Serine	258-261	lin-28 homolog A	Homo sapiens	75-80
31587454-6	2020	We clearly showed the structure-activity relationships of this new class of Lin28-let-7 interaction inhibitors, and confirmed that cellular mature let-7 microRNAs and their target genes could be modulated upon treatment with the pyrazolyl thiazolidinedione-type inhibitor.	Thiazolidinediones	229-256	lin-28 homolog A	Homo sapiens	76-81
30886404-7	2019	We also validate a novel role for the RNA-binding protein LIN28A as an N6-methyladenosine modification "anti-reader".	N-methyladenosine	71-89	lin-28 homolog A	Homo sapiens	58-64
31595560-0	2020	Matrine suppression of self-renewal was dependent on regulation of LIN28A/Let-7 pathway in breast cancer stem cells.	matrine	0-7	lin-28 homolog A	Homo sapiens	67-73
31595560-4	2020	Here we show that the compounds of Kushen injection derived Matrine could suppress the BrCSCs differentiation and self-renewal through downregulating the expression of Lin28A, resulting in the inactivation of Wnt pathway through a Let-7b-dependent way.	matrine	60-67	lin-28 homolog A	Homo sapiens	168-174
31595560-7	2020	Our study uncovers the role of the LIN28A/Let-7 in BrCSCs renewal, and more importantly, elucidated a novel mechanism by which Matrine induces breast cancer involution.	matrine	127-134	lin-28 homolog A	Homo sapiens	35-41
31379107-0	2019	Lin28 enhances de novo fatty acid synthesis to promote cancer progression via SREBP-1.	Fatty Acids	23-33	lin-28 homolog A	Homo sapiens	0-5
31379107-2	2019	Here, we show that both human homologs of Lin28 accelerate de novo fatty acid synthesis and promote the conversion from saturated to unsaturated fatty acids via the regulation of SREBP-1.	Fatty Acids	67-77	lin-28 homolog A	Homo sapiens	42-47
31379107-2	2019	Here, we show that both human homologs of Lin28 accelerate de novo fatty acid synthesis and promote the conversion from saturated to unsaturated fatty acids via the regulation of SREBP-1.	Fatty Acids, Unsaturated	133-156	lin-28 homolog A	Homo sapiens	42-47
31379107-5	2019	Collectively, our findings uncover that post-transcriptional regulation by Lin28A/B enhances de novo fatty acid synthesis and metabolic conversion of saturated and unsaturated fatty acids via SREBP-1, which is critical for cancer progression.	Fatty Acids	101-111	lin-28 homolog A	Homo sapiens	75-83
31379107-5	2019	Collectively, our findings uncover that post-transcriptional regulation by Lin28A/B enhances de novo fatty acid synthesis and metabolic conversion of saturated and unsaturated fatty acids via SREBP-1, which is critical for cancer progression.	saturated and unsaturated fatty acids	150-187	lin-28 homolog A	Homo sapiens	75-83
30833806-12	2019	CONCLUSION: The let-7-related polymorphism rs3811463 in LIN28A is associated with the susceptibility to gastric cancer and the let-7-related polymorphism rs10889677 in IL23R is associated with the prognosis of gastric cancer.	let-7	16-21	lin-28 homolog A	Homo sapiens	56-62
30833806-12	2019	CONCLUSION: The let-7-related polymorphism rs3811463 in LIN28A is associated with the susceptibility to gastric cancer and the let-7-related polymorphism rs10889677 in IL23R is associated with the prognosis of gastric cancer.	let-7	127-132	lin-28 homolog A	Homo sapiens	56-62
29956753-10	2018	In addition, RSV induced the mRNA-decaying activity of TTP and inhibited the relative luciferase activity of baculoviral IAP repeat containing 3 (cIAP2), large tumor suppressor kinase 2 (LATS2), E2F1, and lin-28 homolog A (Lin28) in HCT116 and SNU81 cells.	Resveratrol	13-16	lin-28 homolog A	Homo sapiens	205-221
30234460-7	2018	After screening for suitable combinations of these strategies based on Lin28 expression in co-cultures of fibroblasts and 1 x 104 iPS cells, we found that 1 day of cultivation at 42 C in methionine-free culture medium with or without dinaciclib remarkably decreased Lin28 expression and prevented tumor formation.	Methionine	187-197	lin-28 homolog A	Homo sapiens	266-271
30234460-7	2018	After screening for suitable combinations of these strategies based on Lin28 expression in co-cultures of fibroblasts and 1 x 104 iPS cells, we found that 1 day of cultivation at 42 C in methionine-free culture medium with or without dinaciclib remarkably decreased Lin28 expression and prevented tumor formation.	dinaciclib	234-244	lin-28 homolog A	Homo sapiens	266-271
29956753-10	2018	In addition, RSV induced the mRNA-decaying activity of TTP and inhibited the relative luciferase activity of baculoviral IAP repeat containing 3 (cIAP2), large tumor suppressor kinase 2 (LATS2), E2F1, and lin-28 homolog A (Lin28) in HCT116 and SNU81 cells.	Resveratrol	13-16	lin-28 homolog A	Homo sapiens	223-228
29956753-11	2018	Therefore, RSV enhanced the inhibitory activity of TTP in HCT116 and SNU81 cells by negatively regulating cIAP2, E2F1, LATS2, and Lin28 expression.	Resveratrol	11-14	lin-28 homolog A	Homo sapiens	130-135
30081983-52	2018	Compared to control group, relative mRNA expressions of Lin28, Bax, Bcl-2 and Fas were all higher in worker who were smelting arsenic( P < 0.	Arsenic	126-133	lin-28 homolog A	Homo sapiens	56-61
29552298-0	2018	Synergistic neuroprotective effect of rasagiline and idebenone against retinal ischemia-reperfusion injury via the Lin28-let-7-Dicer pathway.	rasagiline	38-48	lin-28 homolog A	Homo sapiens	115-120
29874593-5	2018	Upon further characterization, we demonstrate that the LIN28 inhibitor TPEN destabilizes the zinc-knuckle domain of LIN28, while LI71 binds the cold shock domain to suppress LIN28"s activity against let-7 in leukemia cells and embryonic stem cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	71-75	lin-28 homolog A	Homo sapiens	55-60
29874593-5	2018	Upon further characterization, we demonstrate that the LIN28 inhibitor TPEN destabilizes the zinc-knuckle domain of LIN28, while LI71 binds the cold shock domain to suppress LIN28"s activity against let-7 in leukemia cells and embryonic stem cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	71-75	lin-28 homolog A	Homo sapiens	116-121
29874593-5	2018	Upon further characterization, we demonstrate that the LIN28 inhibitor TPEN destabilizes the zinc-knuckle domain of LIN28, while LI71 binds the cold shock domain to suppress LIN28"s activity against let-7 in leukemia cells and embryonic stem cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	71-75	lin-28 homolog A	Homo sapiens	116-121
29742265-0	2018	Antiproliferative effect of urolithin A, the ellagic acid-derived colonic metabolite, on hepatocellular carcinoma HepG2.2.15 cells by targeting Lin28a/let-7a axis.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	28-39	lin-28 homolog A	Homo sapiens	144-150
29742265-5	2018	Moreover, urolithin A suppressed the protein expressions of Sp-1, Lin28a, and Zcchc11, and elevated the expression of microRNA let-7a.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	10-21	lin-28 homolog A	Homo sapiens	66-72
29742265-6	2018	Importantly, urolithin A also regulated the Lin28a/let-7a axis in transient HBx-transfected HCC HepG2 cells.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	13-24	lin-28 homolog A	Homo sapiens	44-50
29742265-8	2018	These findings indicated that urolithin A exerted the antiproliferative effect by regulating the Lin28a/let-7a axis and may be a potential supplement for HBV-infected HCC therapy.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	30-41	lin-28 homolog A	Homo sapiens	97-103
29416635-9	2018	In silico analysis suggested that OTUD7B regulation, probably owing to miR-1180 downregulation, may negatively regulate the NF-kappaB-Lin28 axis which in turn triggers Let-7 microRNA-mediated caspase-3 downregulation, thereby conferring paclitaxel resistance in TNBCs.	Paclitaxel	237-247	lin-28 homolog A	Homo sapiens	134-139
29540527-5	2018	We identify truncated domains of Lin28a and of TRBP that are sufficient to support coassociation and mutual elevation of protein levels, and a requirement for MAPK-dependent phosphorylation of TRBP at putative Erk-target serine 152, as well as Lin28a serine 200 phosphorylation, in mediating the increase of Lin28a protein by TRBP.	Serine	221-227	lin-28 homolog A	Homo sapiens	33-39
29540527-5	2018	We identify truncated domains of Lin28a and of TRBP that are sufficient to support coassociation and mutual elevation of protein levels, and a requirement for MAPK-dependent phosphorylation of TRBP at putative Erk-target serine 152, as well as Lin28a serine 200 phosphorylation, in mediating the increase of Lin28a protein by TRBP.	Serine	251-257	lin-28 homolog A	Homo sapiens	33-39
29143345-4	2017	In the present study, alkaline phosphatase activity, alizarin red-positive mineralization, and calcium content, positive indicators of osteogenic differentiation, were significantly higher in cultured human periosteum-derived cells (hPDCs) with Lin28a overexpression compared with cells without Lin28a overexpression.	alizarin	53-65	lin-28 homolog A	Homo sapiens	245-251
29143345-5	2017	Lin28a overexpression by hPDCs also increased mitochondrial activity, which is essential for cellular proliferation, as suggested by a reduced presence of reactive oxygen species and significantly enhanced lactate levels and ATP production.	Reactive Oxygen Species	155-178	lin-28 homolog A	Homo sapiens	0-6
29143345-5	2017	Lin28a overexpression by hPDCs also increased mitochondrial activity, which is essential for cellular proliferation, as suggested by a reduced presence of reactive oxygen species and significantly enhanced lactate levels and ATP production.	Lactic Acid	206-213	lin-28 homolog A	Homo sapiens	0-6
29143345-5	2017	Lin28a overexpression by hPDCs also increased mitochondrial activity, which is essential for cellular proliferation, as suggested by a reduced presence of reactive oxygen species and significantly enhanced lactate levels and ATP production.	Adenosine Triphosphate	225-228	lin-28 homolog A	Homo sapiens	0-6
29552298-0	2018	Synergistic neuroprotective effect of rasagiline and idebenone against retinal ischemia-reperfusion injury via the Lin28-let-7-Dicer pathway.	idebenone	53-62	lin-28 homolog A	Homo sapiens	115-120
29552298-6	2018	Furthermore, idebenone and rasagiline induced the expression of Lin28A and Lin28B, respectively, which resulted in a reduced expression of microRNAs in the let-7 family and an increased protein output of Dicer.	idebenone	13-22	lin-28 homolog A	Homo sapiens	64-70
29552298-6	2018	Furthermore, idebenone and rasagiline induced the expression of Lin28A and Lin28B, respectively, which resulted in a reduced expression of microRNAs in the let-7 family and an increased protein output of Dicer.	rasagiline	27-37	lin-28 homolog A	Homo sapiens	64-70
29201231-4	2017	Let-7 microRNA targets are enriched for genes containing SNPs associated with glucose metabolism, including Lin28.	Glucose	78-85	lin-28 homolog A	Homo sapiens	108-113
29201231-5	2017	In the present study, the effect of T/C variants of rs3811463 (a SNP located near to the let-7 binding site in Lin28) on GDM risk was investigated.	let-7	89-94	lin-28 homolog A	Homo sapiens	111-116
29201231-10	2017	Taken together, it was concluded that the let-7/Lin28 axis regulated glucose uptake and insulin sensitivity by modulating the expression of glucose metabolism-associated proteins.	Glucose	69-76	lin-28 homolog A	Homo sapiens	48-53
29201231-10	2017	Taken together, it was concluded that the let-7/Lin28 axis regulated glucose uptake and insulin sensitivity by modulating the expression of glucose metabolism-associated proteins.	Glucose	140-147	lin-28 homolog A	Homo sapiens	48-53
28910332-0	2017	Concurrent treatment with simvastatin and NF-kappaB inhibitor in human castration-resistant prostate cancer cells exerts synergistic anti-cancer effects via control of the NF-kappaB/LIN28/let-7 miRNA signaling pathway.	Simvastatin	26-37	lin-28 homolog A	Homo sapiens	182-187
28768505-2	2017	Additionally, down-regulation of the let-7 miRNAs in cultured adult CD34(+) cells or the over-expression of LIN28 in cultured erythrocytes from pediatric patients with HbSS genotype causes increased levels of fetal hemoglobin (HbF) in the range of 19-40% of the total.	hbss	168-172	lin-28 homolog A	Homo sapiens	108-113
28671666-6	2017	Conversely, the switch to oligoU requires the ZK domain of Lin28 to drive the formation of a stable ternary complex between pre-let-7 and the inactive LIM.	oligo(U)	26-32	lin-28 homolog A	Homo sapiens	59-64
28235063-2	2017	In the present study, during induction of radio- or chemo-resistance in NSCLC cells, dynamic analyses revealed that decreased expression of let-7 induced by irradiation or cisplatin resulted in increased expression of its target gene LIN28, and increased expression of LIN28 then contributed to further decreased expression of let-7 by inhibiting its maturation and biogenesis.	Cisplatin	172-181	lin-28 homolog A	Homo sapiens	234-239
28587210-0	2017	Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549.	Curcumin	0-8	lin-28 homolog A	Homo sapiens	18-25
28587210-4	2017	Curcumin treatment enhanced the expression of miR-98 and reduced that of the miR-98 target gene LIN28A as well as matrix metalloproteinase (MMP) 2 and MMP9 in vitro and in vivo.	Curcumin	0-8	lin-28 homolog A	Homo sapiens	96-102
28587210-7	2017	Induction of miR-98 by curcumin treatment suppressed MMP2 and MMP9 by targeting LIN28A.	Curcumin	23-31	lin-28 homolog A	Homo sapiens	80-86
28500786-3	2017	We used GB patient cells and cell lines to show that Dov downregulated the stem cell protein Lin28 and its target high-mobility group protein A2 (HMGA2).	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	53-56	lin-28 homolog A	Homo sapiens	93-98
28500786-4	2017	The Dov-induced reduction in pSTAT3Tyr705 phosphorylation demonstrated that Dov negatively affects the STAT3/LIN28/Let-7/HMGA2 regulatory axis in GB cells.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	4-7	lin-28 homolog A	Homo sapiens	109-114
28500786-4	2017	The Dov-induced reduction in pSTAT3Tyr705 phosphorylation demonstrated that Dov negatively affects the STAT3/LIN28/Let-7/HMGA2 regulatory axis in GB cells.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	76-79	lin-28 homolog A	Homo sapiens	109-114
28500786-10	2017	Our results may have immediate clinical implications to improve TMZ response in patients with LIN28+ /HMGA2+ GB, independent of their MGMT methylation status.	Temozolomide	64-67	lin-28 homolog A	Homo sapiens	94-99
28281692-8	2017	Germ cell transcripts POU5F1, TFAP2C, LIN28A, ALPP and KIT were also reduced by ibuprofen.	Ibuprofen	80-89	lin-28 homolog A	Homo sapiens	38-44
28235063-3	2017	Moreover, we showed that down-regulation of let-7 and up-regulation of LIN28 expression promoted resistance to irradiation or cisplatin by regulating the single-cell proliferative capability of NSCLC cells.	Cisplatin	126-135	lin-28 homolog A	Homo sapiens	71-76
26714839-4	2016	METHODS: Sensitivity of LNCaP cells overexpressing Lin28 (LN-Lin28) to enzalutamide, abiraterone, or bicalutamide was compared to that of control LN-neo cells using cell growth assays, proliferation assays using MTT, anchorage-dependent clonogenic ability assays and soft agar assays.	enzalutamide	71-83	lin-28 homolog A	Homo sapiens	51-56
27538419-4	2016	When LIN28A expression was forced and sustained during neural stem cell expansion using an inducible expression-vector system, loss of dopamine neurogenic potential and midbrain phenotypes after long-term culturing was blocked.	Dopamine	135-143	lin-28 homolog A	Homo sapiens	5-11
27681429-9	2016	Together, these results reveal a key role of Wnt-Lin28-let7 miRNA signaling in regulating proliferation and neurogenic potential of MGs in the adult mammalian retina.	1,2-O-DIMETHYL-4-[2,4-DIHYDROXY-BUTYRAMIDO]-4,6-DIDEOXY-ALPHA-D-MANNOPYRANOSIDE	132-135	lin-28 homolog A	Homo sapiens	49-54
27320042-5	2016	Proteomic and metabolomic analysis highlighted roles for LIN28 in maintaining the low mitochondrial function associated with primed pluripotency and in regulating one-carbon metabolism, nucleotide metabolism, and histone methylation.	Carbon	167-173	lin-28 homolog A	Homo sapiens	57-62
26687759-0	2016	Lin28A enhances chemosensitivity of colon cancer cells to 5-FU by promoting apoptosis in a let-7 independent manner.	Fluorouracil	58-62	lin-28 homolog A	Homo sapiens	0-6
26687759-3	2016	In this study, we detected the expression of Lin28A in colon cancer patients and tested the effect of Lin28A on the chemotherapeutic sensitivity of colon cancer cells to 5-fluorouracil (5-FU).	Fluorouracil	170-184	lin-28 homolog A	Homo sapiens	102-108
26687759-5	2016	However, to our surprise, we found that oncogenic protein Lin28A-enforced expression in colon cancer cells enhanced the chemosensitivity of cancer cells to 5-FU via promoting the cell apoptosis.	Fluorouracil	156-160	lin-28 homolog A	Homo sapiens	58-64
26714839-5	2016	Ability of LN-Lin28 cells to maintain AR activation after treatment with enzalutamide, abiraterone, or bicalutamide was tested using immunofluorescence, Western blotting, ChIP assays, and qRT-PCR.	abiraterone	87-98	lin-28 homolog A	Homo sapiens	11-19
26714839-5	2016	Ability of LN-Lin28 cells to maintain AR activation after treatment with enzalutamide, abiraterone, or bicalutamide was tested using immunofluorescence, Western blotting, ChIP assays, and qRT-PCR.	bicalutamide	103-115	lin-28 homolog A	Homo sapiens	11-19
26714839-6	2016	Importance of Lin28 in enzalutamide resistance was assessed by the downregulation of Lin28 expression in C4-2B and 22Rv1 cells chronically treated with enzalutamide.	enzalutamide	23-35	lin-28 homolog A	Homo sapiens	14-19
26714839-6	2016	Importance of Lin28 in enzalutamide resistance was assessed by the downregulation of Lin28 expression in C4-2B and 22Rv1 cells chronically treated with enzalutamide.	enzalutamide	23-35	lin-28 homolog A	Homo sapiens	85-90
26714839-6	2016	Importance of Lin28 in enzalutamide resistance was assessed by the downregulation of Lin28 expression in C4-2B and 22Rv1 cells chronically treated with enzalutamide.	enzalutamide	152-164	lin-28 homolog A	Homo sapiens	14-19
26714839-6	2016	Importance of Lin28 in enzalutamide resistance was assessed by the downregulation of Lin28 expression in C4-2B and 22Rv1 cells chronically treated with enzalutamide.	enzalutamide	152-164	lin-28 homolog A	Homo sapiens	85-90
26714839-9	2016	PCa cells overexpressing Lin28 exhibit resistance to treatment with enzalutamide, abiraterone, or bicalutamide.	enzalutamide	68-80	lin-28 homolog A	Homo sapiens	25-30
26714839-9	2016	PCa cells overexpressing Lin28 exhibit resistance to treatment with enzalutamide, abiraterone, or bicalutamide.	abiraterone	82-93	lin-28 homolog A	Homo sapiens	25-30
26714839-9	2016	PCa cells overexpressing Lin28 exhibit resistance to treatment with enzalutamide, abiraterone, or bicalutamide.	bicalutamide	98-110	lin-28 homolog A	Homo sapiens	25-30
26714839-10	2016	Downregulation of Lin28 resensitizes enzalutamide-resistant PCa cells to enzalutamide treatment.	enzalutamide	37-49	lin-28 homolog A	Homo sapiens	18-23
26714839-10	2016	Downregulation of Lin28 resensitizes enzalutamide-resistant PCa cells to enzalutamide treatment.	enzalutamide	73-85	lin-28 homolog A	Homo sapiens	18-23
26910839-5	2016	Subsequently, LIN28A expression is increased at both mRNA and protein levels in pancreatic cancer cells treated with 5-Aza-2"-deoxycytidine (5-Aza-CdR), a DNA methyltransferase inhibitor.	Decitabine	117-139	lin-28 homolog A	Homo sapiens	14-20
26714839-4	2016	METHODS: Sensitivity of LNCaP cells overexpressing Lin28 (LN-Lin28) to enzalutamide, abiraterone, or bicalutamide was compared to that of control LN-neo cells using cell growth assays, proliferation assays using MTT, anchorage-dependent clonogenic ability assays and soft agar assays.	enzalutamide	71-83	lin-28 homolog A	Homo sapiens	58-66
26714839-4	2016	METHODS: Sensitivity of LNCaP cells overexpressing Lin28 (LN-Lin28) to enzalutamide, abiraterone, or bicalutamide was compared to that of control LN-neo cells using cell growth assays, proliferation assays using MTT, anchorage-dependent clonogenic ability assays and soft agar assays.	abiraterone	85-96	lin-28 homolog A	Homo sapiens	51-56
26714839-4	2016	METHODS: Sensitivity of LNCaP cells overexpressing Lin28 (LN-Lin28) to enzalutamide, abiraterone, or bicalutamide was compared to that of control LN-neo cells using cell growth assays, proliferation assays using MTT, anchorage-dependent clonogenic ability assays and soft agar assays.	bicalutamide	101-113	lin-28 homolog A	Homo sapiens	51-56
26714839-4	2016	METHODS: Sensitivity of LNCaP cells overexpressing Lin28 (LN-Lin28) to enzalutamide, abiraterone, or bicalutamide was compared to that of control LN-neo cells using cell growth assays, proliferation assays using MTT, anchorage-dependent clonogenic ability assays and soft agar assays.	bicalutamide	101-113	lin-28 homolog A	Homo sapiens	58-66
26714839-5	2016	Ability of LN-Lin28 cells to maintain AR activation after treatment with enzalutamide, abiraterone, or bicalutamide was tested using immunofluorescence, Western blotting, ChIP assays, and qRT-PCR.	enzalutamide	73-85	lin-28 homolog A	Homo sapiens	11-19
26944953-2	2016	The expression of Lin28A and AR in formalin-fixed and paraffin-embedded surgical sections from 305 patients with ER-/Her2+ breast cancer was analyzed by immunohistochemistry, and the co-expression patterns in breast cancer cells were investigated by immunofluorescent staining.	Formaldehyde	35-43	lin-28 homolog A	Homo sapiens	18-24
26944953-2	2016	The expression of Lin28A and AR in formalin-fixed and paraffin-embedded surgical sections from 305 patients with ER-/Her2+ breast cancer was analyzed by immunohistochemistry, and the co-expression patterns in breast cancer cells were investigated by immunofluorescent staining.	Paraffin	54-62	lin-28 homolog A	Homo sapiens	18-24
26944953-9	2016	In univariate analysis, Lin28A+/AR+ was significant risk factors associated with unfavorable OS (p = 0.049) and RFS (p = 0.019).	Osmium	93-95	lin-28 homolog A	Homo sapiens	24-30
26711009-5	2016	Mechanistically, Lin28A recruits 5-methylcytosine-dioxygenase Tet1 to genomic binding sites to orchestrate 5-methylcytosine and 5-hydroxymethylcytosine dynamics.	5-Methylcytosine	33-49	lin-28 homolog A	Homo sapiens	17-23
26711009-5	2016	Mechanistically, Lin28A recruits 5-methylcytosine-dioxygenase Tet1 to genomic binding sites to orchestrate 5-methylcytosine and 5-hydroxymethylcytosine dynamics.	5-hydroxymethylcytosine	128-151	lin-28 homolog A	Homo sapiens	17-23
25415050-10	2015	This is the first study to demonstrate that DFMO treatment restores balance to the LIN28/Let-7 axis and inhibits glycolytic metabolism and neurosphere formation in NB and that PET scans may be a meaningful imaging tool to evaluate the therapeutic effects of DFMO treatment.	Eflornithine	44-48	lin-28 homolog A	Homo sapiens	83-88
26675483-4	2015	Transgene expression of LIN28A with a linked puromycin resistance marker was restricted to the erythroid lineage as demonstrated by selective survival of erythroid colonies (greater than 95% of all colonies).	Puromycin	45-54	lin-28 homolog A	Homo sapiens	24-30
26636340-0	2015	Overexpression of Lin28 Decreases the Chemosensitivity of Gastric Cancer Cells to Oxaliplatin, Paclitaxel, Doxorubicin, and Fluorouracil in Part via microRNA-107.	Oxaliplatin	82-93	lin-28 homolog A	Homo sapiens	18-23
26636340-0	2015	Overexpression of Lin28 Decreases the Chemosensitivity of Gastric Cancer Cells to Oxaliplatin, Paclitaxel, Doxorubicin, and Fluorouracil in Part via microRNA-107.	Paclitaxel	95-105	lin-28 homolog A	Homo sapiens	18-23
26636340-0	2015	Overexpression of Lin28 Decreases the Chemosensitivity of Gastric Cancer Cells to Oxaliplatin, Paclitaxel, Doxorubicin, and Fluorouracil in Part via microRNA-107.	Doxorubicin	107-118	lin-28 homolog A	Homo sapiens	18-23
26636340-0	2015	Overexpression of Lin28 Decreases the Chemosensitivity of Gastric Cancer Cells to Oxaliplatin, Paclitaxel, Doxorubicin, and Fluorouracil in Part via microRNA-107.	Fluorouracil	124-136	lin-28 homolog A	Homo sapiens	18-23
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Oxaliplatin	141-152	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Oxaliplatin	154-157	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Paclitaxel	160-170	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Paclitaxel	172-175	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Doxorubicin	178-189	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Doxorubicin	191-194	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Fluorouracil	201-213	lin-28 homolog A	Homo sapiens	45-50
26636340-3	2015	In this study, we found that transfection of Lin28 into gastric cancer cells (MKN45 and MKN28) increased their resistance to the chemo-drugs oxaliplatin (OXA), paclitaxel (PTX), doxorubicin (ADM), and fluorouracil (5-Fu) compared with gastric cancer cells transfected with a control vector.	Fluorouracil	215-219	lin-28 homolog A	Homo sapiens	45-50
25418722-6	2014	Furthermore, our data show that even transient changes in O2 concentration can affect cell fate through HIF by regulating the activity of MYC, a regulator of LIN28/let-7 that is critical for fate decisions in the neural lineage.	Oxygen	58-60	lin-28 homolog A	Homo sapiens	158-163
26045559-3	2015	Here we show that Lin28 target datasets are enriched for RNA sequences predicted to contain stable planar structures of 4 guanines known as G-quartets (G4s).	Guanine	122-130	lin-28 homolog A	Homo sapiens	18-23
26108226-0	2015	Paclitaxel-sensitization enhanced by curcumin involves down-regulation of nuclear factor-kappaB and Lin28 in Hep3B cells.	Paclitaxel	0-10	lin-28 homolog A	Homo sapiens	100-105
26108226-0	2015	Paclitaxel-sensitization enhanced by curcumin involves down-regulation of nuclear factor-kappaB and Lin28 in Hep3B cells.	Curcumin	37-45	lin-28 homolog A	Homo sapiens	100-105
26108226-2	2015	Previously, we discovered that Lin28 was closely associated with resistance to paclitaxel in Hep3B cells.	Paclitaxel	79-89	lin-28 homolog A	Homo sapiens	31-36
26108226-5	2015	In this study, we reported that a combination of curcumin and paclitaxel exhibited synergistic anti-proliferative and pro-apoptosis effects on Hep3B cells, and curcumin down-regulated paclitaxel-induced enhanced expression of Lin28 and NF-kappaB activation.	Curcumin	49-57	lin-28 homolog A	Homo sapiens	226-231
26108226-5	2015	In this study, we reported that a combination of curcumin and paclitaxel exhibited synergistic anti-proliferative and pro-apoptosis effects on Hep3B cells, and curcumin down-regulated paclitaxel-induced enhanced expression of Lin28 and NF-kappaB activation.	Paclitaxel	62-72	lin-28 homolog A	Homo sapiens	226-231
26108226-5	2015	In this study, we reported that a combination of curcumin and paclitaxel exhibited synergistic anti-proliferative and pro-apoptosis effects on Hep3B cells, and curcumin down-regulated paclitaxel-induced enhanced expression of Lin28 and NF-kappaB activation.	Curcumin	160-168	lin-28 homolog A	Homo sapiens	226-231
26108226-5	2015	In this study, we reported that a combination of curcumin and paclitaxel exhibited synergistic anti-proliferative and pro-apoptosis effects on Hep3B cells, and curcumin down-regulated paclitaxel-induced enhanced expression of Lin28 and NF-kappaB activation.	Paclitaxel	184-194	lin-28 homolog A	Homo sapiens	226-231
26108226-6	2015	Furthermore, our results revealed that curcumin reduced Lin28 levels via mechanisms directly mediated by inhibition of NF-kappaB activity.	Curcumin	39-47	lin-28 homolog A	Homo sapiens	56-61
25415050-4	2015	Polyamines, regulated by ornithine decarboxylase (ODC) modulate eIF-5A which is a direct regulator of the LIN28/Let-7 axis.	Polyamines	0-10	lin-28 homolog A	Homo sapiens	106-111
25301052-4	2014	Mechanistically, we discover that Lin28A and Lin28B enhance, whereas let-7 suppresses, aerobic glycolysis via targeting pyruvate dehydrogenase kinase 1, or PDK1, in a hypoxia- or hypoxia-inducible factor-1 (HIF-1)-independent manner, illustrating a novel pathway to mediate aerobic glycolysis of cancer cells even in ambient oxygen levels.	Oxygen	325-331	lin-28 homolog A	Homo sapiens	34-40
24970027-4	2014	We found that the expression of Lin28 was closely associated with resistance to paclitaxel.	Paclitaxel	80-90	lin-28 homolog A	Homo sapiens	32-37
24970027-5	2014	The drug-resistant Hep3B cell line, which expresses high levels of Lin28, is more resistant to paclitaxel and other anticancer drugs than the parental cell line.	Paclitaxel	95-105	lin-28 homolog A	Homo sapiens	67-72
23737330-0	2014	Polyamines are oncometabolites that regulate the LIN28/let-7 pathway in colorectal cancer cells.	Polyamines	0-10	lin-28 homolog A	Homo sapiens	49-54
25112011-5	2014	In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level.	Tretinoin	13-15	lin-28 homolog A	Homo sapiens	180-185
23737330-8	2014	Our findings suggest that polyamines are oncometabolites that influence specific aspects of tumorigenesis by regulating pluripotency associated factors, such as LIN28, via an eIF5A-dependent but let-7-independent mechanism while the expression of proliferation-related genes regulated by let-7, such as HMGA2, is mediated through microRNA mediated repression.	Polyamines	26-36	lin-28 homolog A	Homo sapiens	161-166
23737330-9	2014	Therefore, manipulating polyamine metabolism may be a novel method of targeting the LIN28/let-7 pathway in specific disease states.	Polyamines	24-33	lin-28 homolog A	Homo sapiens	84-89
24356103-0	2014	miR-125b promotes cell proliferation by directly targeting Lin28 in glioblastoma stem cells with low expression levels of miR-125b.	mir-125b	0-8	lin-28 homolog A	Homo sapiens	59-64
24356103-5	2014	Further research into the underlying mechanism demonstrated that miR-125b acts by targeting Lin28 to regulate cell growth.	mir-125b	65-73	lin-28 homolog A	Homo sapiens	92-97
23737330-6	2014	Depletion of polyamines using difluoromethylornithine (DFMO) or genetic knockdown of the polyamine-modified eukaryotic translation initiation factor 5A isoforms 1 and 2 (eIF5A1/2) resulted in robust reduction of both HMGA2 and LIN28.	Polyamines	13-23	lin-28 homolog A	Homo sapiens	227-232
24357531-3	2014	In a recent issue of Cell, Shyh-Chang and colleagues provide experimental evidence that Lin28 prolongs youthful regenerative capacity by increasing oxidative glucose metabolism (Shyh-Chang et al, 2013).	Glucose	158-165	lin-28 homolog A	Homo sapiens	88-93
23939427-4	2013	Both activities strongly depend on Lin28"s RNA-binding domains (RBDs), an N-terminal cold-shock domain (CSD) and a C-terminal Zn-knuckle domain (ZKD).	Zinc	126-128	lin-28 homolog A	Homo sapiens	35-40
24006280-5	2013	Similarly, we observed that LIN28A decreased in ACH-3P cells induced to syncytialize with forskolin treatment.	Colforsin	90-99	lin-28 homolog A	Homo sapiens	28-34
24006280-8	2013	Additionally, targeted degradation of LIN28A mRNA increased responsiveness to forskolin-induced differentiation.	Colforsin	78-87	lin-28 homolog A	Homo sapiens	38-44
22540148-6	2012	Although it is widely considered to be a promiscuous gene expression activator, these results indicated that Aire promotes the self-renewal of ES cells through a specific pathway (i.e., the activation of Lin28 and the inhibition of the let-7 microRNA family).	Einsteinium	143-145	lin-28 homolog A	Homo sapiens	204-209
22547345-9	2013	Furthermore, our data showed that expression of key diabetes susceptibility genes is influenced by HMGA2, which revealed an interesting link to the recently indentified Lin28/let-7 pathway regulating mammalian glucose metabolism.	Glucose	210-217	lin-28 homolog A	Homo sapiens	169-174
23481595-3	2013	In vitro and in vivo, LIN28 preferentially bound single-stranded RNA containing a uridine-rich element and one or more flanking guanosines and appeared to be able to disrupt base-pairing to access these elements when embedded in predicted secondary structure.	Uridine	82-89	lin-28 homolog A	Homo sapiens	22-27
23481595-3	2013	In vitro and in vivo, LIN28 preferentially bound single-stranded RNA containing a uridine-rich element and one or more flanking guanosines and appeared to be able to disrupt base-pairing to access these elements when embedded in predicted secondary structure.	Guanosine	128-138	lin-28 homolog A	Homo sapiens	22-27
23275558-3	2013	We established iPS cell reprogramming of mouse embryonic fibroblasts and human foreskin fibroblasts by transposition of OSKM (Oct4, Sox2, Klf4 and c-Myc) and OSKML (OSKM + Lin28) expression cassettes mobilized by the SB100X hyperactive transposase.	IPS	15-18	lin-28 homolog A	Homo sapiens	172-177
21553022-7	2011	The MTT assay indicated that the proliferation of lung cancer cells with lin-28 inhibition was signally impaired.	monooxyethylene trimethylolpropane tristearate	4-7	lin-28 homolog A	Homo sapiens	73-79
22808086-0	2012	Lin28 mediates paclitaxel resistance by modulating p21, Rb and Let-7a miRNA in breast cancer cells.	Paclitaxel	15-25	lin-28 homolog A	Homo sapiens	0-5
22808086-4	2012	We found that the expression level of Lin28 was closely associated with the resistance to paclitaxel treatment.	Paclitaxel	90-100	lin-28 homolog A	Homo sapiens	38-43
22808086-5	2012	The T47D cancer cell line, which highly expresses Lin28, is more resistant to paclitaxel than the MCF7, Bcap-37 or SK-BR-3 cancer cell lines, which had low-level expression of Lin28.	Paclitaxel	78-88	lin-28 homolog A	Homo sapiens	50-55
22808086-6	2012	Knocking down of Lin28 in Lin28 high expression T47D cells increased the sensitivity to paclitaxel treatment, while stable expression of Lin28 in breast cancer cells effectively attenuated the sensitivity to paclitaxel treatment, resulting in a significant increase of IC50 values of paclitaxel.	Paclitaxel	88-98	lin-28 homolog A	Homo sapiens	17-22
22808086-7	2012	Transfection with Lin28 also significantly inhibited paclitaxel-induced apoptosis.	Paclitaxel	53-63	lin-28 homolog A	Homo sapiens	18-23
22808086-11	2012	Our results indicate that Lin28 expression might be one mechanism underlying paclitaxel resistance in breast cancer, and Lin28 could be a potential target for overcoming paclitaxel resistance in breast cancer.	Paclitaxel	77-87	lin-28 homolog A	Homo sapiens	26-31
22808086-11	2012	Our results indicate that Lin28 expression might be one mechanism underlying paclitaxel resistance in breast cancer, and Lin28 could be a potential target for overcoming paclitaxel resistance in breast cancer.	Paclitaxel	170-180	lin-28 homolog A	Homo sapiens	121-126
22081076-8	2012	These results suggest the possible involvement of LIN28 in regulation of sex steroid dependent cell proliferation of breast carcinoma cells.	Steroids	77-84	lin-28 homolog A	Homo sapiens	50-55
22545159-0	2012	miR-125b promotes early germ layer specification through Lin28/let-7d and preferential differentiation of mesoderm in human embryonic stem cells.	mir-125b	0-8	lin-28 homolog A	Homo sapiens	57-62
22545159-8	2012	Anti-miR-125b inhibitor experiments also showed that miR-125b controls the expression of miRNA let-7d, likely through the negative regulatory effects of Lin28 on let-7.	mir-125b	5-13	lin-28 homolog A	Homo sapiens	153-158
22545159-8	2012	Anti-miR-125b inhibitor experiments also showed that miR-125b controls the expression of miRNA let-7d, likely through the negative regulatory effects of Lin28 on let-7.	mir-125b	53-61	lin-28 homolog A	Homo sapiens	153-158
21962509-0	2011	The Lin28/let-7 axis regulates glucose metabolism.	Glucose	31-38	lin-28 homolog A	Homo sapiens	4-9
21962509-1	2011	The let-7 tumor suppressor microRNAs are known for their regulation of oncogenes, while the RNA-binding proteins Lin28a/b promote malignancy by inhibiting let-7 biogenesis.	let-7	4-9	lin-28 homolog A	Homo sapiens	113-119
21962509-8	2011	These data establish the Lin28/let-7 pathway as a central regulator of mammalian glucose metabolism.	Glucose	81-88	lin-28 homolog A	Homo sapiens	25-30
21912531-3	2011	We initially demonstrated that the T/C variants of rs3811463, a single nucleotide polymorphism (SNP) located near the let-7 binding site in LIN28, could lead to differential regulation of LIN28 by let-7.	let-7	118-123	lin-28 homolog A	Homo sapiens	140-145
21912531-3	2011	We initially demonstrated that the T/C variants of rs3811463, a single nucleotide polymorphism (SNP) located near the let-7 binding site in LIN28, could lead to differential regulation of LIN28 by let-7.	let-7	118-123	lin-28 homolog A	Homo sapiens	188-193
21912531-3	2011	We initially demonstrated that the T/C variants of rs3811463, a single nucleotide polymorphism (SNP) located near the let-7 binding site in LIN28, could lead to differential regulation of LIN28 by let-7.	let-7	197-202	lin-28 homolog A	Homo sapiens	140-145
21912531-3	2011	We initially demonstrated that the T/C variants of rs3811463, a single nucleotide polymorphism (SNP) located near the let-7 binding site in LIN28, could lead to differential regulation of LIN28 by let-7.	let-7	197-202	lin-28 homolog A	Homo sapiens	188-193
34883291-0	2022	Small molecules with tetrahydroquinoline-containing Povarov scaffolds as inhibitors disrupting the Protein-RNA interaction of LIN28-let-7.	1,2,3,4-tetrahydroquinoline	21-40	lin-28 homolog A	Homo sapiens	126-131
17617744-5	2007	In pluripotent mammalian cells, Lin28 is observed in RNase-sensitive complexes with poly(A)-binding protein, and in polysomal fractions of sucrose gradients, suggesting it is associated with translating mRNAs.	Poly A	84-91	lin-28 homolog A	Homo sapiens	32-37
17617744-5	2007	In pluripotent mammalian cells, Lin28 is observed in RNase-sensitive complexes with poly(A)-binding protein, and in polysomal fractions of sucrose gradients, suggesting it is associated with translating mRNAs.	Sucrose	139-146	lin-28 homolog A	Homo sapiens	32-37
34949722-1	2022	The human terminal uridyl transferases TUT4 and TUT7 (TUT4/7) catalyse the additions of uridines at the 3" end of RNAs, including the precursors of the tumour suppressor miRNA let-7 upon recruitment by the oncoprotein LIN28A.	Uridine	88-96	lin-28 homolog A	Homo sapiens	218-224
20670273-6	2010	Reverse transcription-PCR showed that these iPS cells expressed endogenous Oct-3/4, Sox2, Klf4, c-Myc, Nanog and Lin28 genes, whereas all of the transgenes were silenced.	IPS	44-47	lin-28 homolog A	Homo sapiens	113-118
34913237-0	2022	C1632 suppresses the migration and proliferation of non-small-cell lung cancer cells involving LIN28 and FGFR1 pathway.	c1632	0-5	lin-28 homolog A	Homo sapiens	95-100
34913237-3	2022	We found that C1632 could simultaneously inhibit the expression of LIN28 and block FGFR1 signalling transduction in NSCLC A549 and A549R cells, resulting in significant decreases in the phosphorylation of focal adhesion kinase and the expression of matrix metalloproteinase-9.	c1632	14-19	lin-28 homolog A	Homo sapiens	67-72
34911496-3	2021	Cancer de-differentiation transforms luminal-like (differentiated) adenocarcinoma into less luminal-like and more stem-like (undifferentiated) small cell carcinoma through a sequential activation of stem cell transcription factors (scTF) POU5F1, LIN28A, SOX2 and NANOG.	Phenobarbital	37-44	lin-28 homolog A	Homo sapiens	246-252
34655516-7	2021	We demonstrated an example of this by showing that PUM2-induced structure changes on LIN28A enable miR-30 binding.	mir-30	99-105	lin-28 homolog A	Homo sapiens	85-91
34883291-2	2022	Herein, we report the LIN28 inhibitory activities of a series of 30 small molecules with a tricyclic tetrahydroquinoline (THQ)-containing scaffold obtained from a Povarov reaction.	1,2,3,4-tetrahydroquinoline	101-120	lin-28 homolog A	Homo sapiens	22-27
34883291-2	2022	Herein, we report the LIN28 inhibitory activities of a series of 30 small molecules with a tricyclic tetrahydroquinoline (THQ)-containing scaffold obtained from a Povarov reaction.	1,2,3,4-tetrahydroquinoline	122-125	lin-28 homolog A	Homo sapiens	22-27
34136077-0	2021	Trisubstituted Pyrrolinones as Small-Molecule Inhibitors Disrupting the Protein-RNA Interaction of LIN28 and Let-7.	pyrrolinones	15-27	lin-28 homolog A	Homo sapiens	99-104
34868981-5	2021	Overexpression of LIN28A promoted the proliferation and Ara-C chemoresistance of leukemic cells.	Cytarabine	56-61	lin-28 homolog A	Homo sapiens	18-24
34868981-7	2021	In addition, the impacts of LIN28A on cell growth, apoptosis, cell cycle progression, and Ara-C chemoresistance were reverted by the knockdown of CENPE.	Cytarabine	90-95	lin-28 homolog A	Homo sapiens	28-34
34556809-3	2022	Mechanistically, in undifferentiated/proliferating SSCs, LIN28A induced metabolic reprogramming from oxidative phosphorylation (OxPhos) to glycolysis by activating PDK1-mediated glycolysis-TCA/OxPhos uncoupling.	Trichloroacetic Acid	189-192	lin-28 homolog A	Homo sapiens	57-63
34136077-3	2021	Herein, we performed a fluorescence polarization-based screening and identified trisubstituted pyrrolinones as small-molecule inhibitors disrupting the LIN28-let-7 interaction.	pyrrolinones	95-107	lin-28 homolog A	Homo sapiens	152-157
34136077-4	2021	The most potent compound C902 showed dose-dependent inhibition in an EMSA validation assay, enhanced thermal stability of the cold shock domain of LIN28, and increased mature let-7 levels in JAR cells.	c902	25-29	lin-28 homolog A	Homo sapiens	147-152
34136077-6	2021	The pyrrolinones identified in this study not only represent a new class of LIN28-binding molecules that diversify the limited available LIN28 inhibitors but also represent the first examples of small molecules that showed substituent-dependent PRI inhibitory and PPI activating activities.	pyrrolinones	4-16	lin-28 homolog A	Homo sapiens	76-81
34136077-6	2021	The pyrrolinones identified in this study not only represent a new class of LIN28-binding molecules that diversify the limited available LIN28 inhibitors but also represent the first examples of small molecules that showed substituent-dependent PRI inhibitory and PPI activating activities.	pyrrolinones	4-16	lin-28 homolog A	Homo sapiens	137-142
35262736-9	2022	Mutation of the lysine 177 residue of Lin28A to arginine abrogated the ubiquitination and degradation of Lin28A which were accelerated by Kap1 silencing.	Lysine	16-22	lin-28 homolog A	Homo sapiens	38-44
35262736-9	2022	Mutation of the lysine 177 residue of Lin28A to arginine abrogated the ubiquitination and degradation of Lin28A which were accelerated by Kap1 silencing.	Lysine	16-22	lin-28 homolog A	Homo sapiens	105-111
35262736-9	2022	Mutation of the lysine 177 residue of Lin28A to arginine abrogated the ubiquitination and degradation of Lin28A which were accelerated by Kap1 silencing.	Arginine	48-56	lin-28 homolog A	Homo sapiens	38-44
35262736-9	2022	Mutation of the lysine 177 residue of Lin28A to arginine abrogated the ubiquitination and degradation of Lin28A which were accelerated by Kap1 silencing.	Arginine	48-56	lin-28 homolog A	Homo sapiens	105-111