Title : Atorvastatin-induced senescence of hepatocellular carcinoma is mediated by downregulation of hTERT through the suppression of the IL-6/STAT3 pathway.

Pub. Date : 2020

PMID : 32257389






6 Functional Relationships(s)
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1 Atorvastatin-induced senescence of hepatocellular carcinoma is mediated by downregulation of hTERT through the suppression of the IL-6/STAT3 pathway. Atorvastatin interleukin 6 Mus musculus
2 Atorvastatin-induced senescence was independent of p53, p14, and p16, and atorvastatin not only decreased the secretion of IL-6, a major senescence-associated secretory phenotype (SASP) factor, and the phosphorylation of STAT3 but also inhibited the expression of hTERT, a catalytic subunit of telomerase. Atorvastatin interleukin 6 Mus musculus
3 Supplementation with exogenous IL-6 reversed both atorvastatin-induced suppression of STAT3 phosphorylation and hTERT expression and atorvastatin-induced senescence. Atorvastatin interleukin 6 Mus musculus
4 Supplementation with exogenous IL-6 reversed both atorvastatin-induced suppression of STAT3 phosphorylation and hTERT expression and atorvastatin-induced senescence. Atorvastatin interleukin 6 Mus musculus
5 Consistent with these results, atorvastatin decreased the IL-6, p-STAT3, and hTERT levels and increased beta-gal expression in tumor sections. Atorvastatin interleukin 6 Mus musculus
6 Taken together, these data indicate that atorvastatin can induce atypical cellular senescence in HCC cells to inhibit tumor growth, an effect mediated by downregulation of hTERT through suppression of the IL-6/STAT3 pathway. Atorvastatin interleukin 6 Mus musculus