PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34078517-3 2021 High concentration of metformin promoted osteoclast apoptosis and upregulated the expression of Bax/Bcl-2 and caspase-3; BV/TV, BS/TV, Tb.N and BMD were increased while Tp.Sp decreased in the group of intraperitoneal metformin+femoral intramedullary osteoclast injection (Met+OC) compared with the control group, 1 nM metformin downregulated Akt, p44/42 MAPK, JNK, p38 MAPK phosphorylation, 5 nM metformin down regulated ERK and Akt phosphorylation. Metformin 22-31 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 34164906-6 2021 In metformin-treated cells, MALAT1 knock-down increased the Bax/Bcl2 ratio and enhanced p21 but decreased cyclin B1 expression. Metformin 3-12 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 34078517-3 2021 High concentration of metformin promoted osteoclast apoptosis and upregulated the expression of Bax/Bcl-2 and caspase-3; BV/TV, BS/TV, Tb.N and BMD were increased while Tp.Sp decreased in the group of intraperitoneal metformin+femoral intramedullary osteoclast injection (Met+OC) compared with the control group, 1 nM metformin downregulated Akt, p44/42 MAPK, JNK, p38 MAPK phosphorylation, 5 nM metformin down regulated ERK and Akt phosphorylation. Metformin 217-226 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 34078517-3 2021 High concentration of metformin promoted osteoclast apoptosis and upregulated the expression of Bax/Bcl-2 and caspase-3; BV/TV, BS/TV, Tb.N and BMD were increased while Tp.Sp decreased in the group of intraperitoneal metformin+femoral intramedullary osteoclast injection (Met+OC) compared with the control group, 1 nM metformin downregulated Akt, p44/42 MAPK, JNK, p38 MAPK phosphorylation, 5 nM metformin down regulated ERK and Akt phosphorylation. Metformin 318-327 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 29274299-7 2018 Although metformin significantly upregulated the protein levels of the pro-apoptotic markers cleaved-caspase 3 and Bax in Jurkat cells, rosiglitazone did not have such an effect. Metformin 9-18 BCL2 associated X, apoptosis regulator Homo sapiens 115-118 33268288-9 2021 Moreover, western blotting assay revealed that metformin could decrease Hcy-induced expression of Bax and cleaved caspase3, and increase the expression of Bcl-2. Metformin 47-56 BCL2 associated X, apoptosis regulator Homo sapiens 98-101 32657143-8 2021 In the metformin treated group, the expression of Bax and PUMA genes was enhanced while the expression of Bcl-2, hTERT, mTOR, and p53 genes declined. Metformin 7-16 BCL2 associated X, apoptosis regulator Homo sapiens 50-53 32657143-9 2021 Although all treatments induced apoptosis, the combination of curcumin and metformin showed the maximum level of apoptosis, cytotoxicity, and expression of Bax gene. Metformin 75-84 BCL2 associated X, apoptosis regulator Homo sapiens 156-159 30088260-14 2018 Finally, we found that metformin may modulate the pro-apoptotic Bax, anti-apoptotic Bcl-2, MMP-2, MMP-9, miR-21 and miR-155 expression levels. Metformin 23-32 BCL2 associated X, apoptosis regulator Homo sapiens 64-67 29897998-6 2018 Results showed that combination treatment with liraglutide (100 nmol/L) and metformin (0.75 mmol/L) significantly decreased cell viability and colony formation, caused cell cycle arrest, upregulated the level of pro-apoptotic proteins Bax and cleaved caspase-3, and inhibited cell migration in the cells, although their single treatment did not exhibit such effects. Metformin 76-85 BCL2 associated X, apoptosis regulator Homo sapiens 235-238 33886150-7 2021 We found that cotreatment with metformin (30 mM) and pitavastatin (10 muM) significantly reduced cell viability; caused G0/G1 cell cycle arrest; upregulated the expression levels of Bax, PCNA, cleaved PARP-1, cleaved caspase-3, LC3 II, and p27 Kip1 /p21Cip1 ; and inhibited cell migration. Metformin 31-40 BCL2 associated X, apoptosis regulator Homo sapiens 182-185 33758522-6 2021 T2DM on metformin group had significantly higher Bad, Bax, and caspase-7 expression. Metformin 8-17 BCL2 associated X, apoptosis regulator Homo sapiens 54-57 33758522-8 2021 Metformin treatment significantly inhibited the expression of Bcl-10, Bid, and caspase-3 and upregulated Bad/Bax/caspase-7 pathway suggesting the activation of Bad/Bax/caspase-7 apoptotic pathway. Metformin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 109-112 33758522-8 2021 Metformin treatment significantly inhibited the expression of Bcl-10, Bid, and caspase-3 and upregulated Bad/Bax/caspase-7 pathway suggesting the activation of Bad/Bax/caspase-7 apoptotic pathway. Metformin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 32792943-8 2020 The presence of metformin also sensitized NSCLC cells to celecoxib-induced apoptosis by activating caspase-9, -8, -3, and -7, upregulating the pro-apoptotic proteins Bad and Bax, and downregulating the antiapoptotic proteins Bcl-xl and Bcl-2. Metformin 16-25 BCL2 associated X, apoptosis regulator Homo sapiens 174-177 32495867-10 2020 Moreover, Metformin treatment groups (0, 20, and 40 mM) had more apoptotic PANC-1 cells, higher expression levels of pro-apoptosis proteins Caspase-3 and Bax and lower expression levels of anti-apoptosis protein Bcl-2 and the mTOR pathway-related proteins PI3K, p-Akt, and p-mTOR in cells than Control group (p<0.05). Metformin 10-19 BCL2 associated X, apoptosis regulator Homo sapiens 154-157 31220411-3 2019 We found that metformin decreased the cell apoptosis rate and death, ratio of Bcl-2/Bax, and expression of NR2A and NR2B, and increased the expression of LC3 in Abeta25-35 -treated SH-SY5Y cells. Metformin 14-23 BCL2 associated X, apoptosis regulator Homo sapiens 84-87 31173255-8 2019 In addition, compared with the control group, metformin significantly enhanced the activity of caspase-3, increased the expression of AMPK/pAMPK/Bax proteins and reduced the expression of mTOR/Bcl-2 proteins (P<0.05). Metformin 46-55 BCL2 associated X, apoptosis regulator Homo sapiens 145-148 31014173-6 2019 Here we show that while metformin can significantly inhibit cell growth and induce apoptosis of OSCC cultured alone in a dose-dependent manner through activating p-AMPKT172 and modulating Bcl-2, Bax, and cleaved PARP. Metformin 24-33 BCL2 associated X, apoptosis regulator Homo sapiens 195-198 30625181-6 2019 Similarly, metformin treatment suppressed expressions of anti-apoptotic genes BCL2 and Bcl-xL, and mesenchymal genes vimentin, N-cadherin, Zeb1 and Zeb2 with simultaneous enhancement of apoptotic caspase 3 and Bax, and epithelial genes E-cadherin and keratin 19 expressions, confirming an inhibitory effect of metformin in tumorigenesis. Metformin 11-20 BCL2 associated X, apoptosis regulator Homo sapiens 210-213 30481793-7 2018 RESULTS: We found that metformin significantly inhibited proliferation and induced apoptosis of both ESCC cell lines in a dose- and time-dependent manner, and the expression of Bcl-2 was down-regulated and Bax and Caspase-3 were up-regulated. Metformin 23-32 BCL2 associated X, apoptosis regulator Homo sapiens 206-209 29399562-5 2018 In addition, mRNA expression of pro-apoptotic genes, p21 and Bax, was decreased and of anti-apoptotic genes, Bcl-2 and Bcl-xl, was increased with metformin treatment compared to QUIN-induced cells. Metformin 146-155 BCL2 associated X, apoptosis regulator Homo sapiens 61-64 26111693-6 2015 The expressions of caspase-3 and Bax protein were significantly increased (P<0.05) and Bcl-2 protein expression was decreased (P<0.05) with a lowered Bcl-2/Bax ratio in AGEs-treated fibroblasts (P<0.05), and such changes were significantly reversed by metformin treatment (P<0.05). Metformin 261-270 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 29212192-5 2017 The results showed that vorinostat combined with gefitinib augmented BIM expression and increased the sensitivity of EGFR-TKI resistant NSCLC cells to gefitinib, adding metformin simultaneously could obviously inhibit the expression of anti-apoptotic proteins, and further increased expression levels of BIM and BAX, and as a result, further improved the sensitivity of gefitinib both on the NSCLC cells with intrinsic and acquired resistance to EGFR-TKI. Metformin 169-178 BCL2 associated X, apoptosis regulator Homo sapiens 312-315 27371846-6 2016 LP1 promoted the downregulated expression of Bcl-2 and the upregulated expression of Bax induced by metformin, but it didn"t show any impact on the metformin-activated AMPK pathway. Metformin 100-109 BCL2 associated X, apoptosis regulator Homo sapiens 85-88 26266765-9 2015 Metformin induced apoptosis by down-regulating Bcl-2 and Bcl-xL expression, and up-regulating Bax and Cytochrome c expression. Metformin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 26225749-5 2015 Treatment of MCF-7 cells with metformin or phenformin induced increase in p53 protein levels and the transcription of its downstream target genes, Bax and p21, in a dose-dependent manner. Metformin 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 147-150 29085821-7 2017 Additionally, metformin increased the expression levels of p53, Bax, Bad while it reduced expression levels of Akt, Bcl-2, and Mdm2. Metformin 14-23 BCL2 associated X, apoptosis regulator Homo sapiens 64-67 28927780-9 2017 The combination of specific inhibitors of ERK1/2, JNK or PI3K/Akt pathway and metformin further promoted cell apoptosis and the up-regulation of p21, Bax, Bad, cleaved caspase-3 and -9 as well as the down-regulation of Bcl-2 mediated by metformin alone, but inhibition of p38 pathway exhibited the opposite results. Metformin 78-87 BCL2 associated X, apoptosis regulator Homo sapiens 150-153 27082123-6 2016 Consistently, Bax and Bim were upregulated in metformin-treated cells. Metformin 46-55 BCL2 associated X, apoptosis regulator Homo sapiens 14-17 26111693-7 2015 CONCLUSION: Metformin can antagonize AGEs-induced apoptosis in human dermal fibroblasts by regulating the expressions of caspase-3, Bax and Bcl-2. Metformin 12-21 BCL2 associated X, apoptosis regulator Homo sapiens 132-135 24612549-9 2014 In addition, these tamoxifen-induced effects that were enhanced by metformin may be involved in the bax/bcl-2 apoptotic pathway and the AMPK/mTOR/p70S6 growth pathway. Metformin 67-76 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 24858012-8 2014 In MCF-7 cells metformin decreased the activation of IRbeta, Akt and ERK1/2, increased p-AMPK, FOXO3a, p27, Bax and cleaved caspase-3, and decreased phosphorylation of p70S6K and Bcl-2 protein expression. Metformin 15-24 BCL2 associated X, apoptosis regulator Homo sapiens 108-111 26117007-5 2015 In process of inducing effect of 20 mmol/L metformin on THP-1 cells, the expressions of BCL-XL and BIM did not significantly changed, while the expressions of BAX and caspase-3 significantly increased (P<0.01). Metformin 43-52 BCL2 associated X, apoptosis regulator Homo sapiens 159-162 23151022-12 2012 In addition, metformin induced apoptosis in OSCC cells, significantly down-regulating the anti-apoptotic proteins Bcl-2 and Bcl-xL and up-regulating the pro-apoptotic protein Bax. Metformin 13-22 BCL2 associated X, apoptosis regulator Homo sapiens 175-178 21776823-5 2011 Metformin induced apoptosis by arresting cells in G1 phase and reducing cyclin D level and increasing the expression of p21 and cyclin E. Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2. Metformin 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 225-228 21388661-6 2011 Moreover, we established that metformin can induce apoptosis in OVCAR-3 and OVCAR-4 cells by activating caspases 3/7, down-regulating Bcl-2 and Bcl-xL expression, and up-regulating Bax and Bad expression. Metformin 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 181-184 21776823-8 2011 Furthermore, MEK inhibitor significantly suppressed metformin-induced p53 and Bax elevation while ERK inhibitor generated a slight reduction in p53 levels. Metformin 52-61 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 21776823-11 2011 All these results suggested that metformin activated p53, Bax, and induced tumor cell apoptosis through the ERK signaling pathway. Metformin 33-42 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 21776823-5 2011 Metformin induced apoptosis by arresting cells in G1 phase and reducing cyclin D level and increasing the expression of p21 and cyclin E. Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2. Metformin 184-193 BCL2 associated X, apoptosis regulator Homo sapiens 225-228