LNCaP公司
前列腺癌
胰腺癌
癌症研究
活力测定
辛伐他汀
低密度脂蛋白
细胞生长
前列腺
内科学
化学
细胞凋亡
癌症
胆固醇
内分泌学
车站3
医学
生物化学
作者
Young Yun Jung,Jeong‐Hyeon Ko,Jae‐Young Um,Arunachalam Chinnathambi,Sulaiman Ali Alharbi,Gautam Sethi,Kwang Seok Ahn
摘要
Abstract Hypercholesterolemia has been found to be closely linked with a significant increase in both cancer incidence and mortality. However, the exact correlation between serum cholesterol levels and cancer has not been completely deciphered. Here we analyzed the effect of low‐density lipoprotein (LDL) cholesterol on prostate and pancreatic cancer cells. We noted that LDL induced a substantial STAT3 activation and JAK1, JAK2, Src activation in diverse prostate and pancreatic tumor cells. Moreover, LDL promoted cancer cell proliferation, migration, and invasion as well as upregulated the expression of diverse oncogenic gene products. However, deletion of LDL‐activated STAT3 in LNCaP and PANC‐1 cells and reduced LDL‐induced cell viability. Simvastatin (SV) treatment also alleviated LDL‐induced cell viability and migration ability in both the prostate and pancreatic tumor cells. These results demonstrate that LDL‐induced STAT3 activation may exert a profound effect on the proliferation and survival of tumor cells.
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