Department of Science in Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Department of Botany and Microbiology, King Saud University, Riyadh, Kingdom of Saudi Arabia.
J Cell Physiol. 2021 Jul;236(7):5253-5264. doi: 10.1002/jcp.30229. Epub 2020 Dec 23.
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.
高胆固醇血症与癌症发病率和死亡率的显著增加密切相关。然而，血清胆固醇水平与癌症的确切相关性尚未完全阐明。在这里，我们分析了低密度脂蛋白（LDL）胆固醇对前列腺癌和胰腺癌细胞的影响。我们注意到，LDL 诱导了不同前列腺癌和胰腺癌肿瘤细胞中 STAT3 的显著激活以及 JAK1、JAK2、Src 的激活。此外，LDL 促进了癌细胞的增殖、迁移和侵袭，并上调了多种致癌基因产物的表达。然而，LNCaP 和 PANC-1 细胞中 LDL 激活的 STAT3 的缺失以及 LDL 诱导的细胞活力降低。辛伐他汀（SV）治疗也减轻了前列腺和胰腺肿瘤细胞中 LDL 诱导的细胞活力和迁移能力。这些结果表明，LDL 诱导的 STAT3 激活可能对肿瘤细胞的增殖和存活产生深远影响。
