Kim Jeong Nam, Kim Tae Hun, Yoon Ji-Hye, Cho Sung-Gook
Department of Microbiology, College of Natural Sciences, Pusan National University, Pusan, Republic of Korea.
Department of Biotechnology, Korea National University of Transportation, Chungbuk, Republic of Korea.
Anticancer Res. 2018 Oct;38(10):5791-5798. doi: 10.21873/anticanres.12918.
BACKGROUND/AIM: The aim of the present study was to investigate the mechanism through which kisspeptin inhibits colorectal cancer metastasis.
Colorectal cancer cells were treated with kisspeptin and then subjected to assays for cell viability, migration, invasion and anchorage-independent growth. Kisspeptin receptor (KISS1R) requirement was examined by siRNA-based gene silencing followed by western blot and invasion assays. Kisspeptin regulation of PKR and PP2A was examined by treating cells with inhibitors for PKR or PP2A.
Kisspeptin inhibited colorectal cancer cell invasiveness without affecting cell proliferation. Kisspeptin required activation of KISS1R and resulted in activation of PKR and PP2A. PKR inhibitor blocked kisspeptin-induced PP2A phosphorylation, while PP2A inhibitor failed to block kisspeptin-induced PKR phosphorylation.
Kisspeptin-mediated activation of PKR-PP2A inhibited colorectal cancer cell invasiveness.
背景/目的：本研究旨在探究亲吻素抑制结直肠癌转移的机制。
用亲吻素处理结直肠癌细胞，然后进行细胞活力、迁移、侵袭和非锚定依赖性生长检测。通过基于小干扰RNA的基因沉默，随后进行蛋白质印迹和侵袭检测，来研究亲吻素受体（KISS1R）的必要性。用PKR或PP2A抑制剂处理细胞，检测亲吻素对PKR和PP2A的调节作用。
亲吻素抑制结直肠癌细胞的侵袭性，但不影响细胞增殖。亲吻素需要激活KISS1R，并导致PKR和PP2A的激活。PKR抑制剂可阻断亲吻素诱导的PP2A磷酸化，而PP2A抑制剂未能阻断亲吻素诱导的PKR磷酸化。
亲吻素介导的PKR-PP2A激活抑制了结直肠癌细胞的侵袭性。
