PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12434292-8 2002 In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells. Lovastatin 39-49 KRAS proto-oncogene, GTPase Homo sapiens 156-161 19760159-0 2010 Lovastatin overcomes gefitinib resistance in human non-small cell lung cancer cells with K-Ras mutations. Lovastatin 0-10 KRAS proto-oncogene, GTPase Homo sapiens 89-94 19760159-11 2010 Taken together, these results suggest lovastatin can overcome gefitinib resistance, in NSCLC cells with K-Ras mutations, by down regulation of RAS protein, which leads to inhibition of both RAF/ERK and AKT pathways. Lovastatin 38-48 KRAS proto-oncogene, GTPase Homo sapiens 104-109 16156861-5 2005 However, combinations of FTI and GGTI or lovastatin were found to synergistically inhibit MM cell proliferation, migration, K- and N-RAS processing, RAS-to-mitogen-activated protein kinase signalling and to induce apoptosis. Lovastatin 41-51 KRAS proto-oncogene, GTPase Homo sapiens 124-136 34873318-0 2021 Author Correction: Autophagy inhibitors increase the susceptibility of KRAS-mutant human colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and lovastatin. Lovastatin 162-172 KRAS proto-oncogene, GTPase Homo sapiens 71-75 8672984-4 1995 Also, agents such as perillyl alcohol and lovastatin that interfere with protein isoprenylation and, hence, inhibit oncogene activation may protect against aberrant K-ras expression. Lovastatin 42-52 KRAS proto-oncogene, GTPase Homo sapiens 165-170 11879577-8 2002 The increased steroid hormone production in mutant K-ras-transfected cells was reversed by lovastatin, a pharmacologic inhibitor of p21ras function. Lovastatin 91-101 KRAS proto-oncogene, GTPase Homo sapiens 51-56 9472115-0 1998 Lovastatin inhibits proliferation of pancreatic cancer cell lines with mutant as well as with wild-type K-ras oncogene but has different effects on protein phosphorylation and induction of apoptosis. Lovastatin 0-10 KRAS proto-oncogene, GTPase Homo sapiens 104-109 33608672-0 2021 Autophagy inhibitors increase the susceptibility of KRAS-mutant human colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and lovastatin. Lovastatin 143-153 KRAS proto-oncogene, GTPase Homo sapiens 52-56 33608672-4 2021 In this study we investigated the effect of a combination of 2-deoxy-D-glucose with lovastatin (a known inhibitor of mevalonate pathway and oxidative phosphorylation) on growth of KRAS-mutant human colorectal cancer cell lines HCT116 and LoVo. Lovastatin 84-94 KRAS proto-oncogene, GTPase Homo sapiens 180-184