GANT61 Modulates Autophagy and Lipid Metabolism in Ovarian Cancer.

IF 5.9 1区生物学 Q2 CELL BIOLOGY

Cell Proliferation Pub Date : 2025-05-01 DOI:10.1111/cpr.70051

Yibin Pan, Lingfeng Chen, Jinlu Shen, Shihao Hong, Xiaojing Guan, Xudong Ma, Rongrong Tang, Meifei Lu, Fangying Sun, Shanliang Shang, Yongdong Dai, Zhaokai Zhou, Songying Zhang, Jianhua Yang

引用次数: 0

Abstract

GANT61 induced autophagy via the AKT pathway and promoted the accumulation of lipid droplets in both cell lines. The molecular mechanism behind this lipid accumulation appears to involve the mediation of SREBP1. Furthermore, the combination of GANT61 with CQ/Fatostatin significantly inhibited the proliferation and clonogenicity of SKOV3 and SKOV3PTX cells.

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GANT61调节卵巢癌自噬和脂质代谢。

GANT61通过AKT通路诱导细胞自噬，促进脂滴在两种细胞系中的积累。脂质积累背后的分子机制似乎涉及SREBP1的介导。此外，GANT61与CQ/Fatostatin联合使用可显著抑制SKOV3和SKOV3PTX细胞的增殖和克隆性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Proliferation 生物-细胞生物学

CiteScore

14.80

自引率

2.40%

发文量

198

审稿时长

1 months

期刊介绍： Cell Proliferation Focus: Devoted to studies into all aspects of cell proliferation and differentiation. Covers normal and abnormal states. Explores control systems and mechanisms at various levels: inter- and intracellular, molecular, and genetic. Investigates modification by and interactions with chemical and physical agents. Includes mathematical modeling and the development of new techniques. Publication Content: Original research papers Invited review articles Book reviews Letters commenting on previously published papers and/or topics of general interest By organizing the information in this manner, readers can quickly grasp the scope, focus, and publication content of Cell Proliferation.