Page 31 - 南京医科大学学报自然科学版

第43卷第11期 南京医科大学学报（自然科学版）
2023年11月 Journal of Nanjing Medical University（Natural Sciences） ·1503 ·

·基础研究·

RGFP966通过PI3K/AKT通路抑制胃癌细胞增殖

董正宇 ，张先稳 ，张 林 2
3*
1，2
扬州大学医学院，江苏 扬州 225001；盐城市第二人民医院肿瘤内科，江苏 盐城 224003；扬州大学附属苏北人民医院
1 2 3
肿瘤科，江苏 扬州 225001

［摘 要］ 目的：探讨组蛋白去乙酰化酶3特异性抑制剂RGFP966对胃癌细胞增殖能力和细胞周期的影响及其作用机制。方
法：采用CCK⁃8法检测RGFP966处理MKN⁃45和MGC⁃803细胞后各组细胞的活力；细胞克隆形成实验检测RGFP966对胃癌细
胞集落形成能力的影响；流式细胞术检测细胞周期；Western blot 实验检测细胞增殖和周期相关蛋白 Ki⁃67、c⁃Myc、Cyclin
A2、Cyclin D1 以及 PI3K/AKT 信号通路相关蛋白的表达情况。结果：与对照组相比，RGFP966 可显著抑制胃癌细胞 MKN⁃45
和 MGC⁃803的增殖能力、集落形成能力。与对照组相比，流式细胞术显示RGFP966诱导胃癌细胞阻滞在G0/G1期。与对照组
相比，RGFP966处理后细胞增殖和周期相关蛋白Ki⁃67、c⁃Myc、Cyclin A2、Cyclin D1表达均下降，RGFP966可显著降低PI3K和
AKT的磷酸化水平。结论：RGFP966抑制胃癌细胞的增殖能力并诱导胃癌细胞阻滞在G0/G1期，其作用机制可能与RGFP966
抑制PI3K/AKT信号通路有关。
［关键词］ RGFP966；胃癌细胞；增殖；PI3K/AKT
［中图分类号］ R735.2 ［文献标志码］ A ［文章编号］ 1007⁃4368（2023）11⁃1503⁃06
doi：10.7655/NYDXBNS20231104

RGFP966 inhibits the proliferation of gastric cancer cells through PI3K/AKT pathway

1，2
3*
DONG Zhengyu ，ZHANG Xianwen ，ZHANG Lin 2
Medical College of Yangzhou University，Yangzhou 225001；Department of Oncology，Yancheng Second People’s
1 2
Hospital，Yancheng 224003；Department of Oncology，North Jiangsu People’s Hospital Affiliated to Yangzhou
3
University，Yangzhou 225001，China

［Abstract］ Objective：The objective of the current study was to investigate the effects of RGFP966，a histone deacetylase 3
inhibitor，on the proliferation and cell cycle of gastric cancer cells，as well as its underlying mechanism. Methods：The activity of MKN⁃
45 and MGC⁃803 cell lines treated with RGFP966 was assessed using the CCK⁃8 method. The cytoclonal ability of gastric cancer cells
in response to RGFP966 was examined using a cell cloning assay. Flow cytometry was employed to analyze the cell cycle distribution.
The protein expressions of Ki⁃67，c⁃Myc，Cyclin A2，Cyclin D1，and the PI3K/AKT signaling pathway were evaluated through Western
blot analysis. Results：Compared with the control group，RGFP966 significantly inhibited the proliferation and clonal ability of MKN⁃
45 and MGC⁃803 gastric cancer cells. Flow cytometry analysis revealed that RGFP966 induced cell cycle arrest at the G0/G1 phase.
Furthermore，treatment with RGFP966 resulted in reduced levels of the proliferation ⁃ related proteins Ki ⁃ 67 and c ⁃ Myc，as well as
decreased expressions of Cyclin A2 and Cyclin D1. Moreover，RGFP966 significantly suppressed the phosphorylation levels of PI3K
and AKT. Conclusion：Our findings indicate that RGFP966 inhibits the proliferation of gastric cancer cells and induces cell cycle
arrest at the G0/G1 phase. These effects may be attributed to the inhibition of the PI3K/AKT signaling pathway by RGFP966.
［Key words］ RGFP966；gastric cancer cells；proliferation；PI3K/AKT
［J Nanjing Med Univ，2023，43（11）：1503⁃1508］

胃癌是我国最常见的恶性肿瘤之一，早期胃癌

［基金项目］ 江苏省自然科学基金（BK20211115） 常无明显症状，临床症状明显时常已进展到晚期，
［1］
∗ 因此病死率极高 。胃癌的发病机制较复杂，目前
通信作者（Corresponding author），E⁃mail：zhangxwwok@163.com