PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33992804-8 2021 Collectively, our study uncovers simvastatin as a potential therapeutic drug for immunotherapy in CRC, which suppresses lncRNA SNHG29 mediated YAP activation and promotes anti-tumor immunity by inhibiting PD-L1 expression. Simvastatin 33-44 Yes1 associated transcriptional regulator Homo sapiens 143-146 30536599-0 2019 Simvastatin and the Rho-kinase inhibitor Y-27632 prevent myofibroblast transformation in Peyronie"s disease-derived fibroblasts via inhibition of YAP/TAZ nuclear translocation. Simvastatin 0-11 Yes1 associated transcriptional regulator Homo sapiens 146-149 32210573-0 2020 Simvastatin Inhibits the Malignant Behaviors of Gastric Cancer Cells by Simultaneously Suppressing YAP and beta-Catenin Signaling. Simvastatin 0-11 Yes1 associated transcriptional regulator Homo sapiens 99-102 32210573-7 2020 Mechanistic studies showed that simvastatin treatment could inhibit the expression of beta-catenin and the activity of YAP and the downstream targets of YAP and beta-catenin in gastric cancer cells. Simvastatin 32-43 Yes1 associated transcriptional regulator Homo sapiens 119-122 32210573-7 2020 Mechanistic studies showed that simvastatin treatment could inhibit the expression of beta-catenin and the activity of YAP and the downstream targets of YAP and beta-catenin in gastric cancer cells. Simvastatin 32-43 Yes1 associated transcriptional regulator Homo sapiens 153-156 32210573-9 2020 Further investigation revealed that simvastatin mainly acted through by inhibiting the activity of RhoA to inhibit YAP and beta-catenin, and the geranylgeranyl pyrophosphate pathway mediated this regulation. Simvastatin 36-47 Yes1 associated transcriptional regulator Homo sapiens 115-118 31100067-2 2019 Exposure of sparse cultures of PANC-1 and MiaPaCa-2 cells to cerivastatin or simvastatin induced a striking re-localization of YAP from the nucleus to the cytoplasm and inhibited the expression of the YAP/TEAD-regulated genes Connective Tissue Growth Factor (CTGF) and Cysteine-rich angiogenic inducer 61 (CYR61). Simvastatin 77-88 Yes1 associated transcriptional regulator Homo sapiens 127-130 31100067-2 2019 Exposure of sparse cultures of PANC-1 and MiaPaCa-2 cells to cerivastatin or simvastatin induced a striking re-localization of YAP from the nucleus to the cytoplasm and inhibited the expression of the YAP/TEAD-regulated genes Connective Tissue Growth Factor (CTGF) and Cysteine-rich angiogenic inducer 61 (CYR61). Simvastatin 77-88 Yes1 associated transcriptional regulator Homo sapiens 201-204 30536599-14 2019 In our experiments, Rho-kinase inhibition and simvastatin treatment were shown to prevent this in TGF-beta1-stimulated cells on an RNA and protein level through the inhibition of YAP/TAZ nuclear translocation. Simvastatin 46-57 Yes1 associated transcriptional regulator Homo sapiens 179-182 30106444-6 2018 The combination of simvastatin and EGFR inhibitors inhibited YAP and EGFR signaling more markedly than each agent alone. Simvastatin 19-30 Yes1 associated transcriptional regulator Homo sapiens 61-64 30106444-7 2018 Adding back geranylgeranyl pyrophosphate (GGPP), a key product of the mevalonate pathway, reversed the YAP bioactivity inhibition induced by simvastatin and the cell proliferation inhibition induced by the combination of simvastatin and EGFR inhibitors. Simvastatin 141-152 Yes1 associated transcriptional regulator Homo sapiens 103-106 29316250-9 2018 These observations were confirmed with cultured tumor fragments prepared from patients with TNBC after treatment with Wnt inhibitor ICG-001 and YAP inhibitor simvastatin. Simvastatin 158-169 Yes1 associated transcriptional regulator Homo sapiens 144-147 29449645-7 2018 Combined targeting of YAP and EGFR signaling by simvastatin and the EGFR signaling inhibitors, including the EGFR tyrosine kinase inhibitor (TKI) gefitinib, the RAF inhibitor sorafenib and the MEK inhibitor trametinib, presented strong synergistic cytotoxicities in HCC cells. Simvastatin 48-59 Yes1 associated transcriptional regulator Homo sapiens 22-25 33032653-0 2020 Synergistic antitumor interaction of valproic acid and simvastatin sensitizes prostate cancer to docetaxel by targeting CSCs compartment via YAP inhibition. Simvastatin 55-66 Yes1 associated transcriptional regulator Homo sapiens 141-144 30106444-5 2018 Simvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor of the mevalonate pathway that inhibits YAP bioactivity through nuclear translocation and total YAP expression, increased the cytotoxicity of EGFR inhibitors (cetuximab and gefitinib) against CRC cells. Simvastatin 0-11 Yes1 associated transcriptional regulator Homo sapiens 123-126 30106444-5 2018 Simvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor of the mevalonate pathway that inhibits YAP bioactivity through nuclear translocation and total YAP expression, increased the cytotoxicity of EGFR inhibitors (cetuximab and gefitinib) against CRC cells. Simvastatin 0-11 Yes1 associated transcriptional regulator Homo sapiens 179-182 30015955-0 2018 Low-frequency ultrasound and microbubbles combined with simvastatin promote the apoptosis of MCF-7 cells by affecting the LATS1/YAP/RHAMM pathway. Simvastatin 56-67 Yes1 associated transcriptional regulator Homo sapiens 128-131 30015955-8 2018 Furthermore, it was confirmed that LFU and microbubbles combined with simvastatin affected the large tumor suppressor 1 (LATS1)/yes-associated protein (YAP)/receptor of the hyaluronan-mediated motility (RHAMM) pathway in MCF-7 cells. Simvastatin 70-81 Yes1 associated transcriptional regulator Homo sapiens 152-155 30015955-10 2018 In conclusion, the results of the present study indicate that LFU and microbubbles combined with simvastatin promotes the apoptosis of MCF-7 cells via the LATS1/YAP/RHAMM pathway. Simvastatin 97-108 Yes1 associated transcriptional regulator Homo sapiens 161-164 24367099-5 2014 Here we show that RHAMM expression is regulated by mevalonate and Hippo pathways converging onto Yes-associated protein (YAP)/TEAD, which binds RHAMM promoter at specific sites and controls its transcription and consequently breast cancer cell migration and invasion (BCCMI); and that simvastatin inhibits BCCMI via targeting YAP-mediated RHAMM transcription. Simvastatin 285-296 Yes1 associated transcriptional regulator Homo sapiens 97-119 24367099-5 2014 Here we show that RHAMM expression is regulated by mevalonate and Hippo pathways converging onto Yes-associated protein (YAP)/TEAD, which binds RHAMM promoter at specific sites and controls its transcription and consequently breast cancer cell migration and invasion (BCCMI); and that simvastatin inhibits BCCMI via targeting YAP-mediated RHAMM transcription. Simvastatin 285-296 Yes1 associated transcriptional regulator Homo sapiens 121-124 24367099-5 2014 Here we show that RHAMM expression is regulated by mevalonate and Hippo pathways converging onto Yes-associated protein (YAP)/TEAD, which binds RHAMM promoter at specific sites and controls its transcription and consequently breast cancer cell migration and invasion (BCCMI); and that simvastatin inhibits BCCMI via targeting YAP-mediated RHAMM transcription. Simvastatin 285-296 Yes1 associated transcriptional regulator Homo sapiens 326-329 24367099-6 2014 Required for ERK phosphorylation and BCCMI, YAP-activated RHAMM transcription is dependent on mevalonate and sensitive to simvastatin, which modulate RHAMM transcription by modulating YAP phosphorylation and nuclear-cytoplasmic localization. Simvastatin 122-133 Yes1 associated transcriptional regulator Homo sapiens 44-47 24367099-6 2014 Required for ERK phosphorylation and BCCMI, YAP-activated RHAMM transcription is dependent on mevalonate and sensitive to simvastatin, which modulate RHAMM transcription by modulating YAP phosphorylation and nuclear-cytoplasmic localization. Simvastatin 122-133 Yes1 associated transcriptional regulator Homo sapiens 184-187 24367099-7 2014 Further, modulation by mevalonate/simvastatin of YAP-activated RHAMM transcription requires geranylgeranylation, Rho GTPase activation, and actin cytoskeleton rearrangement, but is largely independent of MST and LATS kinase activity. Simvastatin 34-45 Yes1 associated transcriptional regulator Homo sapiens 49-52