PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31686512-8 2019 Using the kinase inhibitor, Sorafenib as a model drug, it is shown that HMP-lipid fragments containing the drug can efficiently enter a hepatocellular carcinoma cell line (Huh 7.5), indicating the use of such fragments as drug delivery nanocarriers. Sorafenib 28-37 MIR7-3 host gene Homo sapiens 172-177 31465134-2 2019 In this study, we first produced three sorafenib resistance (SR) HCC cell lines by using two human HCC cell lines (Hep3B and Huh7) and a human primary HCC cell line. Sorafenib 39-48 MIR7-3 host gene Homo sapiens 125-129 31385002-10 2019 RESULTS: The combination of sorafenib and CMG002 additively inhibited Huh-7 and HepG2 cell proliferation compared to single-agent treatment. Sorafenib 28-37 MIR7-3 host gene Homo sapiens 70-75 29251327-3 2018 The differences in signaling pathway characteristics under sorafenib treatment between HCC (HLF, Huh7, PLC/PRF/5) and CCC (RBE, YSCCC, Huh28) cell lines were therefore investigated using cell proliferation, western blotting, and apoptosis analyses. Sorafenib 59-68 MIR7-3 host gene Homo sapiens 97-101 30476722-4 2019 Huh7 cells were used in the present study and the cell apoptosis and migration were determined in response to sorafenib treatment. Sorafenib 110-119 MIR7-3 host gene Homo sapiens 0-4 30127933-3 2018 The present study aimed to evaluate the potency of apoptosis-induction by As2O3/sorafenib treatment in HCC cell lines, Huh7, 97H and freshly-isolated HCC cells, and also to elucidate the underlying mechanism. Sorafenib 80-89 MIR7-3 host gene Homo sapiens 119-123 30127933-10 2018 The combination of As2O3 and sorafenib had anti-proliferative and pro-apoptotic effects in the liver cancer cell line, Huh7, via increased expression of TRAIL, but not in 97H cells. Sorafenib 29-38 MIR7-3 host gene Homo sapiens 119-123 30127933-13 2018 Overall, the combination of As2O3 and sorafenib demonstrated potent anti-tumor activity in Huh7 and freshly-isolated HCC cells via a TRAIL-dependent pathway. Sorafenib 38-47 MIR7-3 host gene Homo sapiens 91-95 29805309-8 2018 Here, we show that liver cancer cells also exhibit heterogeneous sensitivities to sorafenib induced cell death, which co-relates with the STAT3-Y705 phosphorylation levels and JAK1/2 expression levels in Hep3B, Huh7 and HepG2 cells. Sorafenib 82-91 MIR7-3 host gene Homo sapiens 211-215 30765873-7 2019 We confirmed sorafenib resistance to be associated with EMT and enhanced motility in both HuH7-SR and SKHep-1-SR cells documenting a 4-fold increase in Axl phosphorylation as an adaptive feature of chronic sorafenib treatment in SKHep-1-SR cells. Sorafenib 13-22 MIR7-3 host gene Homo sapiens 90-94 30321984-3 2018 Here, we demonstrate that emodin significantly improved the anti-cancer effect of sorafenib in HCC cells, such as HepG2, Hep3B, Huh7, SK-HEP-1, and PLC/PRF5. Sorafenib 82-91 MIR7-3 host gene Homo sapiens 128-132 28833396-4 2018 In this study, we generated two functionally distinct sorafenib-resistant human Huh-7 HCC cell lines in order to identify new mechanisms to abrogate acquired SR as well as new potential therapeutic targets in HCC. Sorafenib 54-63 MIR7-3 host gene Homo sapiens 80-85 28833396-7 2018 Furthermore, miR-7 effectively silenced TYRO3 expression in both sorafenib-sensitive and sorafenib-resistant Huh-7 cells, inhibiting TYRO3/growth arrest specific 6-mediated cancer cell migration and invasion. Sorafenib 89-98 MIR7-3 host gene Homo sapiens 109-114 28874716-8 2017 The large Huh7 cell spheroids containing HUVECs survived at higher concentrations of anti-cancer drugs (doxorubicin and sorafenib) than did monolayer cells. Sorafenib 120-129 MIR7-3 host gene Homo sapiens 10-14 28900541-7 2017 Using Hep3B and HuH7 HCC cells, it was demonstrated that sorafenib and aspirin acted synergistically to induce apoptosis. Sorafenib 57-66 MIR7-3 host gene Homo sapiens 16-20 27982429-4 2017 Looking for a potential microRNA-based mechanism of action of the drug, we found that sorafenib increases cellular expression of miR-125a in cultured HuH-7 and HepG2 HCC cells. Sorafenib 86-95 MIR7-3 host gene Homo sapiens 150-155 27184800-5 2016 RESULTS: We observed that genes of the metallothionein-1 (MT1) family are induced in the HCC cell line Huh7 exposed to sorafenib. Sorafenib 119-128 MIR7-3 host gene Homo sapiens 103-107 28414325-9 2017 Sorafenib significantly inhibited the viability of all subpopulations except the Huh-7-DN subpopulation. Sorafenib 0-9 MIR7-3 host gene Homo sapiens 81-86 28414325-10 2017 Compared with other sorafenib-sensitive subpopulations, the Huh-7-DN subpopulation showed enhanced expression of Hh transcription factor Gli-2 and ABCC1 transporter protein. Sorafenib 20-29 MIR7-3 host gene Homo sapiens 60-65 27484637-4 2016 Cell viability was reduced by sorafenib from 1 mumol/L in HepG2 or HuH7 cells, and 2.5 mumol/L in Hep3B cells. Sorafenib 30-39 MIR7-3 host gene Homo sapiens 67-71 27484637-5 2016 Co-administration of melatonin and sorafenib exhibited a synergistic cytotoxic effect on HepG2 and HuH7 cells, while Hep3B cells displayed susceptibility to doses of sorafenib that had no effect when administrated alone. Sorafenib 35-44 MIR7-3 host gene Homo sapiens 99-103 28350139-6 2017 In the present study, we found that adenine nucleotide translocator 2 (ANT2) was upregulated in sorafenib-resistant HCC Huh7 cells (Huh7-R) and its overexpression promoted sorafenib resistance. Sorafenib 96-105 MIR7-3 host gene Homo sapiens 120-124 28350139-6 2017 In the present study, we found that adenine nucleotide translocator 2 (ANT2) was upregulated in sorafenib-resistant HCC Huh7 cells (Huh7-R) and its overexpression promoted sorafenib resistance. Sorafenib 96-105 MIR7-3 host gene Homo sapiens 132-136 28350139-6 2017 In the present study, we found that adenine nucleotide translocator 2 (ANT2) was upregulated in sorafenib-resistant HCC Huh7 cells (Huh7-R) and its overexpression promoted sorafenib resistance. Sorafenib 172-181 MIR7-3 host gene Homo sapiens 120-124 28350139-9 2017 miR-137 was downregulated in the Huh7-R cells, compared with that in the Huh7 cells and its restoration reversed sorafenib resistance in the Huh7-R cells. Sorafenib 113-122 MIR7-3 host gene Homo sapiens 33-37 28350139-9 2017 miR-137 was downregulated in the Huh7-R cells, compared with that in the Huh7 cells and its restoration reversed sorafenib resistance in the Huh7-R cells. Sorafenib 113-122 MIR7-3 host gene Homo sapiens 73-77 28350139-9 2017 miR-137 was downregulated in the Huh7-R cells, compared with that in the Huh7 cells and its restoration reversed sorafenib resistance in the Huh7-R cells. Sorafenib 113-122 MIR7-3 host gene Homo sapiens 73-77 27367026-5 2016 MTS assay found that SIRT3 overexpression sensitized liver cancer cells to chemotherapeutic agents and sorafenib in SMMC-7721, Huh-7 and PLC/PRF/5 cell lines. Sorafenib 103-112 MIR7-3 host gene Homo sapiens 127-132 25463538-10 2015 In turn, sorafenib lowered mCD163 and IGF-1 release by M2 macrophages, which decelerated M2 macrophage driven HuH7 and HepG2 proliferation by 47% and 64%, respectively. Sorafenib 9-18 MIR7-3 host gene Homo sapiens 110-114 26790028-4 2016 In this study, we established sorafenib-resistant cells from Huh7 and Mahlavu cell lines by long-term sorafenib exposure. Sorafenib 30-39 MIR7-3 host gene Homo sapiens 61-65 26790028-4 2016 In this study, we established sorafenib-resistant cells from Huh7 and Mahlavu cell lines by long-term sorafenib exposure. Sorafenib 102-111 MIR7-3 host gene Homo sapiens 61-65 26460271-5 2015 Sorafenib and 5-FU treatment decreased growth rates in Huh7 and Huh-BAT cells; however, the treatments exerted different effects in SP cells and on the expression levels of JNK signaling molecules. Sorafenib 0-9 MIR7-3 host gene Homo sapiens 55-59 26516583-5 2015 In the present study, we combined sorafenib with FTY720 in order to sensitize the HCC cell lines Huh7 and HepG2 to sorafenib treatment. Sorafenib 34-43 MIR7-3 host gene Homo sapiens 97-101 26516583-5 2015 In the present study, we combined sorafenib with FTY720 in order to sensitize the HCC cell lines Huh7 and HepG2 to sorafenib treatment. Sorafenib 115-124 MIR7-3 host gene Homo sapiens 97-101 26516583-7 2015 Further studies in Huh7 revealed that combined treatment with FTY720 and sorafenib resulted in G1 arrest and enhanced cell death measured using flow cytometry analysis of cells labeled with propidium iodide (PI)/Annexin-V and PI and 4",6-diamidino-2-phenylindole-staining of nuclei. Sorafenib 73-82 MIR7-3 host gene Homo sapiens 19-23 25850433-4 2015 To identify target proteins associated with the development of sorafenib resistance, we applied stable isotope labelling with amino acids in cell culture (SILAC)-based quantitative proteomic approach to analyze differences in protein expression levels between parental HuH-7 and sorafenib-acquired resistance HuH-7 (HuH-7(R)) cells in vitro, combined with an isobaric tags for relative and absolute quantitation (iTRAQ) quantitative analysis of HuH-7 and HuH-7(R) tumors in vivo. Sorafenib 63-72 MIR7-3 host gene Homo sapiens 269-274 25850433-4 2015 To identify target proteins associated with the development of sorafenib resistance, we applied stable isotope labelling with amino acids in cell culture (SILAC)-based quantitative proteomic approach to analyze differences in protein expression levels between parental HuH-7 and sorafenib-acquired resistance HuH-7 (HuH-7(R)) cells in vitro, combined with an isobaric tags for relative and absolute quantitation (iTRAQ) quantitative analysis of HuH-7 and HuH-7(R) tumors in vivo. Sorafenib 63-72 MIR7-3 host gene Homo sapiens 309-314 25850433-4 2015 To identify target proteins associated with the development of sorafenib resistance, we applied stable isotope labelling with amino acids in cell culture (SILAC)-based quantitative proteomic approach to analyze differences in protein expression levels between parental HuH-7 and sorafenib-acquired resistance HuH-7 (HuH-7(R)) cells in vitro, combined with an isobaric tags for relative and absolute quantitation (iTRAQ) quantitative analysis of HuH-7 and HuH-7(R) tumors in vivo. Sorafenib 63-72 MIR7-3 host gene Homo sapiens 316-324 25850433-4 2015 To identify target proteins associated with the development of sorafenib resistance, we applied stable isotope labelling with amino acids in cell culture (SILAC)-based quantitative proteomic approach to analyze differences in protein expression levels between parental HuH-7 and sorafenib-acquired resistance HuH-7 (HuH-7(R)) cells in vitro, combined with an isobaric tags for relative and absolute quantitation (iTRAQ) quantitative analysis of HuH-7 and HuH-7(R) tumors in vivo. Sorafenib 63-72 MIR7-3 host gene Homo sapiens 309-314 25850433-4 2015 To identify target proteins associated with the development of sorafenib resistance, we applied stable isotope labelling with amino acids in cell culture (SILAC)-based quantitative proteomic approach to analyze differences in protein expression levels between parental HuH-7 and sorafenib-acquired resistance HuH-7 (HuH-7(R)) cells in vitro, combined with an isobaric tags for relative and absolute quantitation (iTRAQ) quantitative analysis of HuH-7 and HuH-7(R) tumors in vivo. Sorafenib 63-72 MIR7-3 host gene Homo sapiens 455-463 24692700-5 2014 RESULTS: FH535 and sorafenib caused inhibition of Huh7 and LCSC. Sorafenib 19-28 MIR7-3 host gene Homo sapiens 50-54 25349646-9 2014 Immunoblotting analysis revealed a marked increase in SFN-mediated autophagy flux in Huh7 cells, which was, however, absent in Hep3B cells. Sorafenib 54-57 MIR7-3 host gene Homo sapiens 85-89 23877009-11 2013 In vivo, sorafenib and PX-866 or regorafenib and MK2206 cooperated to suppress the growth of established HuH7 and HCT116 tumors, respectively. Sorafenib 9-18 MIR7-3 host gene Homo sapiens 105-109 25057499-12 2014 CONCLUSIONS: HSC-LX2 coculture induced sorafenib resistance in Huh7 through multiple pathways: HGF/c-Met/Akt pathway and Jak2/Stat3 pathway. Sorafenib 39-48 MIR7-3 host gene Homo sapiens 63-67 23769634-9 2013 Interestingly, HuH7 cells were more sensitive to sorafenib than LCSC or PLC cells. Sorafenib 49-58 MIR7-3 host gene Homo sapiens 15-19 23769634-10 2013 Additionally, combination therapy with PKI-587 and sorafenib caused significantly more inhibition than monotherapy in HuH7, PLC, and LCSC. Sorafenib 51-60 MIR7-3 host gene Homo sapiens 118-122 23543326-11 2014 RESULTS: Both sorafenib and proteasome inhibitors induced apoptosis in Huh7 and OUMS29. Sorafenib 14-23 MIR7-3 host gene Homo sapiens 71-75 23543326-14 2014 Sorafenib induced down-regulation of Akt synergistically in combination with proteasome inhibitors in Huh7. Sorafenib 0-9 MIR7-3 host gene Homo sapiens 102-106 23543326-16 2014 In addition, sorafenib also inhibited proteasome inhibitor-mediated JNK and p38 activation in both Huh7 and OUMS29. Sorafenib 13-22 MIR7-3 host gene Homo sapiens 99-103 25057499-0 2014 Hepatic stellate cell coculture enables sorafenib resistance in Huh7 cells through HGF/c-Met/Akt and Jak2/Stat3 pathways. Sorafenib 40-49 MIR7-3 host gene Homo sapiens 64-68 25057499-2 2014 We assessed whether HSC-LX2 coculture conferred sorafenib resistance in Huh7 and revealed the mechanism underlying the drug resistance. Sorafenib 48-57 MIR7-3 host gene Homo sapiens 72-76 25057499-3 2014 EXPERIMENTAL DESIGN: The effect of LX2 on sorafenib resistance was determined by coculture system with Huh7 cells. Sorafenib 42-51 MIR7-3 host gene Homo sapiens 103-107 25057499-6 2014 RESULTS: LX2 coculture significantly induced sorafenib resistance in Huh7 by activating p-Akt that led to reactivation of p-ERK. Sorafenib 45-54 MIR7-3 host gene Homo sapiens 69-73 22811581-8 2012 Sorafenib decreased Wnt signaling and beta-catenin protein in HepG2 (CTNNB1 class), SNU387 (Wnt-TGFbeta class), SNU398 (CTNNB1-mutation), and Huh7 (lithium-chloride-pathway activation) cell lines. Sorafenib 0-9 MIR7-3 host gene Homo sapiens 142-146 23724146-5 2013 METHODOLOGY/PRINCIPAL FINDINGS: In vitro, rhASM/sorafenib treatment reduced the viability of Huh7 liver cancer cells more than sorafenib. Sorafenib 48-57 MIR7-3 host gene Homo sapiens 93-97 23724146-11 2013 CONCLUSIONS/SIGNIFICANCE: The rhASM/sorafenib combination exhibited a synergistic effect on reducing the tumor volume and blood vessel density in Huh7 xenografts, despite modest activity of rhASM in these tumors. Sorafenib 36-45 MIR7-3 host gene Homo sapiens 146-150 22801548-4 2012 Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading to sorafenib-induced HCC cell-growth inhibition. Sorafenib 173-182 MIR7-3 host gene Homo sapiens 36-40 22801548-5 2012 Sorafenib inhibited cell growth in both cell lines in a dose- and time-dependent manner and significantly altered expression levels of 826 and 2011 transcripts in HepG2 and Huh7 cells, respectively. Sorafenib 0-9 MIR7-3 host gene Homo sapiens 173-177 22261591-2 2012 This study aimed to test the inhibitory effects of PKI-587 and sorafenib as single agents or in combination on HCC (Huh7 cell line) proliferation. Sorafenib 63-72 MIR7-3 host gene Homo sapiens 116-120 21858812-4 2012 Sorafenib treatment led to accumulation of autophagosomes as evidenced by conversion from LC3-I to LC3-II observed by immunoblot in Huh7, HLF and PLC/PRF/5 cells. Sorafenib 0-9 MIR7-3 host gene Homo sapiens 132-136 22261591-6 2012 Combination of PKI-587 and sorafenib was a more effective inhibitor of Huh7 proliferation than the combination of PI-103 and sorafenib. Sorafenib 27-36 MIR7-3 host gene Homo sapiens 71-75 22261591-7 2012 Combination of PKI-587 and sorafenib synergistically inhibited epidermal growth factor (EGF)-stimulated Huh7 proliferation compared with monodrug therapy. Sorafenib 27-36 MIR7-3 host gene Homo sapiens 104-108 21205925-3 2011 In this study, we established two sorafenib-resistant HCC cell lines from Huh7, a human HCC cell line, by long-term exposure of cells to sorafenib. Sorafenib 34-43 MIR7-3 host gene Homo sapiens 74-78 22753710-8 2012 RESULTS: Our in vitro study found that combination of sorafenib and PI-103 additively inhibited Huh7 proliferation as compared to single-agent treatment. Sorafenib 54-63 MIR7-3 host gene Homo sapiens 96-100 21205925-4 2011 Sorafenib induced significant apoptosis in Huh7 cells; however, Huh7-R1 and Huh7-R2 showed significant resistance to sorafenib-induced apoptosis at the clinical relevant concentrations (up to 10 muM). Sorafenib 0-9 MIR7-3 host gene Homo sapiens 43-47 21205925-4 2011 Sorafenib induced significant apoptosis in Huh7 cells; however, Huh7-R1 and Huh7-R2 showed significant resistance to sorafenib-induced apoptosis at the clinical relevant concentrations (up to 10 muM). Sorafenib 117-126 MIR7-3 host gene Homo sapiens 64-68 21205925-4 2011 Sorafenib induced significant apoptosis in Huh7 cells; however, Huh7-R1 and Huh7-R2 showed significant resistance to sorafenib-induced apoptosis at the clinical relevant concentrations (up to 10 muM). Sorafenib 117-126 MIR7-3 host gene Homo sapiens 64-68 21205925-5 2011 Thorough comparisons of the molecular changes between Huh7 and resistant cells showed that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway played a significant role in mediating acquired resistance to sorafenib in Huh7-R1 and Huh7-R2 cells. Sorafenib 216-225 MIR7-3 host gene Homo sapiens 54-58 21205925-5 2011 Thorough comparisons of the molecular changes between Huh7 and resistant cells showed that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway played a significant role in mediating acquired resistance to sorafenib in Huh7-R1 and Huh7-R2 cells. Sorafenib 216-225 MIR7-3 host gene Homo sapiens 229-233 21205925-5 2011 Thorough comparisons of the molecular changes between Huh7 and resistant cells showed that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway played a significant role in mediating acquired resistance to sorafenib in Huh7-R1 and Huh7-R2 cells. Sorafenib 216-225 MIR7-3 host gene Homo sapiens 229-233 21205925-7 2011 In addition, ectopic expression of constitutive Akt in Huh7 demonstrated similar resistance to sorafenib. Sorafenib 95-104 MIR7-3 host gene Homo sapiens 55-59 21205925-8 2011 The knockdown of Akt by RNA interference reversed resistance to sorafenib in Huh7-R1 cells, indicating the importance of Akt in drug sensitivity. Sorafenib 64-73 MIR7-3 host gene Homo sapiens 77-81 21187475-2 2010 This study reports how sorafenib (a multi-kinase inhibitor) and PI-103 (a dual PI3K/mTOR inhibitor) alone and in combination inhibit the proliferation of the HCC cell line, Huh7. Sorafenib 23-32 MIR7-3 host gene Homo sapiens 173-177 21187475-12 2010 CONCLUSION: The combination of sorafenib and PI-103 can significantly inhibit EGF-stimulated Huh7 proliferation by blocking both Ras/Raf/MAPK and PI3K/AKT/mTOR pathways. Sorafenib 31-40 MIR7-3 host gene Homo sapiens 93-97 21187475-5 2010 RESULTS: Sorafenib and PI-103, as single agents inhibited Huh7 proliferation and epidermal growth factor (EGF)-stimulated Huh7 proliferation in a dose-dependent fashion; the combination of sorafenib and PI-103 produced synergistic effects. Sorafenib 9-18 MIR7-3 host gene Homo sapiens 58-62 32724415-5 2020 Sorafenib inhibited the proliferation of the Li-7, Hep3B, HepG2 and Huh7 liver cancer cell lines (effective group), but not that of the HLE, HLF and ALEX cancer cell lines (non-effective group). Sorafenib 0-9 MIR7-3 host gene Homo sapiens 68-72 33234725-2 2020 In the present study, RNA was extracted from sorafenib-resistant and -sensitive clones of the HCC cell lines HepG2 and Huh7. Sorafenib 45-54 MIR7-3 host gene Homo sapiens 119-123 34634203-2 2021 Notably, the trimeric compound exhibited antihepatoma cytotoxicity more potent than that of sorafenib with IC50 values of 6.2 muM (HepG2), 6.8 muM (Huh7), and 7.2 muM (SK-HEP-1). Sorafenib 92-101 MIR7-3 host gene Homo sapiens 148-152 34366674-3 2021 We here analyzed the response of two HCC cell lines representative of different virus-related etiology, namely Hep3B (HBV+) and HUH7 (permissive to HCV replication) to sorafenib treatment. Sorafenib 168-177 MIR7-3 host gene Homo sapiens 128-132 34159680-3 2021 We established a sorafenib-resistant Huh7 (human HCC) cell line, and characterized it with cytokine assays, then developed CAFs by co-culturing human hepatic stellate cells with resistant or parental Huh7 cells. Sorafenib 17-26 MIR7-3 host gene Homo sapiens 37-41 34159680-5 2021 The sorafenib-resistant Huh7 (Huh7SR ) cells expressed increased B-cell activating factor (BAFF), which promoted highly expression of CAF specific markers in Huh7SR -co-cultured CAFs, showed activated BAFF, BAFF-R and downstream NFkappaB-Nrf2 pathway, and aggravated invasion, migration and drug resistance in co-cultured Huh7 cells. Sorafenib 4-13 MIR7-3 host gene Homo sapiens 24-28 34159680-5 2021 The sorafenib-resistant Huh7 (Huh7SR ) cells expressed increased B-cell activating factor (BAFF), which promoted highly expression of CAF specific markers in Huh7SR -co-cultured CAFs, showed activated BAFF, BAFF-R and downstream NFkappaB-Nrf2 pathway, and aggravated invasion, migration and drug resistance in co-cultured Huh7 cells. Sorafenib 4-13 MIR7-3 host gene Homo sapiens 30-36 34159680-5 2021 The sorafenib-resistant Huh7 (Huh7SR ) cells expressed increased B-cell activating factor (BAFF), which promoted highly expression of CAF specific markers in Huh7SR -co-cultured CAFs, showed activated BAFF, BAFF-R and downstream NFkappaB-Nrf2 pathway, and aggravated invasion, migration and drug resistance in co-cultured Huh7 cells. Sorafenib 4-13 MIR7-3 host gene Homo sapiens 158-164 34159680-5 2021 The sorafenib-resistant Huh7 (Huh7SR ) cells expressed increased B-cell activating factor (BAFF), which promoted highly expression of CAF specific markers in Huh7SR -co-cultured CAFs, showed activated BAFF, BAFF-R and downstream NFkappaB-Nrf2 pathway, and aggravated invasion, migration and drug resistance in co-cultured Huh7 cells. Sorafenib 4-13 MIR7-3 host gene Homo sapiens 322-326 32699265-5 2021 We showed that artesunate greatly enhanced the anticancer effects of low dose of sorafenib against Huh7, SNU-449, and SNU-182 HCC cell lines in vitro and against Huh7 cell xenograft model in Balb/c nude mice. Sorafenib 81-90 MIR7-3 host gene Homo sapiens 99-103 32699265-5 2021 We showed that artesunate greatly enhanced the anticancer effects of low dose of sorafenib against Huh7, SNU-449, and SNU-182 HCC cell lines in vitro and against Huh7 cell xenograft model in Balb/c nude mice. Sorafenib 81-90 MIR7-3 host gene Homo sapiens 162-166 32210579-9 2020 Results: In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 129-138 MIR7-3 host gene Homo sapiens 149-153 32210579-9 2020 Results: In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 129-138 MIR7-3 host gene Homo sapiens 155-159 32210579-9 2020 Results: In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 129-138 MIR7-3 host gene Homo sapiens 155-159 32210579-9 2020 Results: In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 129-138 MIR7-3 host gene Homo sapiens 149-153 32210579-9 2020 Results: In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 129-138 MIR7-3 host gene Homo sapiens 155-159 32210579-9 2020 Results: In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 129-138 MIR7-3 host gene Homo sapiens 155-159 32210579-10 2020 Furthermore, we demonstrated that miR-29b could directly interact with HANR and abolished HANR-induced sorafenib resistance by suppressing autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 103-112 MIR7-3 host gene Homo sapiens 167-171 32149026-4 2020 Besides, based on GO (Gene Ontology) term enrichment analysis, these differentially expressed lncRNAs are mainly related to binding and catalytic activity and biological regulation of metabolic processes in both the sorafenib-resistant Huh7 cells (Huh7-S) and sorafenib-resistant HepG2 cells (HepG2-S) compared to the parental cells. Sorafenib 216-225 MIR7-3 host gene Homo sapiens 236-240 32149026-4 2020 Besides, based on GO (Gene Ontology) term enrichment analysis, these differentially expressed lncRNAs are mainly related to binding and catalytic activity and biological regulation of metabolic processes in both the sorafenib-resistant Huh7 cells (Huh7-S) and sorafenib-resistant HepG2 cells (HepG2-S) compared to the parental cells. Sorafenib 260-269 MIR7-3 host gene Homo sapiens 236-240 32169577-9 2020 Established sorafenib-resistant Huh1 and Huh7 cell lines showed reduced expression of Capicua without mutations. Sorafenib 12-21 MIR7-3 host gene Homo sapiens 41-45