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MOLECULAR MECHANISMS ANTI-PROLIFERATIVE EFFECT OF STATINS IN OSCC CELLS: UPREGULATION OF P21/P27, INHIBITION OF DNMT1, AND FEEDBACK RESPONSE MEDIATED BY SREBP2

為了解決SUZUKI 0800的問題，作者Rachmad Anres Dongoran 這樣論述：

Statins, known as HMG-CoA reductase inhibitors (HMGCR), are a class of cholesterol-lowering drugs and their anti-cancer effects have been studied in different types of malignant diseases. In the present study, we investigated the anti-proliferative effects of statins, including cerivastatin and sim

vastatin, on oral squamous cell carcinoma (OSCC) cells. Our data showed that statins inhibited the proliferation of three OSCC cell lines in a dose- and time-dependent manner and this growth inhibition was confirmed through G0/G1 cell cycle arrest. Accordingly, we found the upregulation of cell cycl

e-related tumor suppressor genes p21 and p27 and downregulation of cyclin-dependent kinases, CDK2, CDK4, and CDK6. Statins are HMGCR inhibitors and 5’ adenosine monophosphate-activated protein kinase (AMPK) activators, in contrast, AMPK and its phosphorylation form were downregulated, on the other h

and, HMGCR and the other related genes such as HMGCS1, LDLR1, FASN, and PCSK9 were paradoxically increased as a feedback response mediated by SREBP2 upregulation. Importantly, we are the first to clearly show that statins were able to inhibit DNA methyltransferase 1 (DNMT1) and further promote the u

pregulation of p21 transcriptionally in OSCC cells. Statins also decreased SKP2 expression resulted in p21 and p27 protein accumulation by preventing their proteasomal degradation. Taken together, our data clearly showed that the anti-proliferative effect of statins is mediated by suppressing DNMT1

and SKP2 expression, thus promoting p21 and p27 expression and leading to G0/G1 cell cycle arrest in OSCC cells.