抑制自噬可增强能量限制诱导的肝癌细胞死亡。

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
IUBMB Life Pub Date : 2024-03-18 DOI:10.1002/iub.2816
Sara M. Elgendy, Dana M. Zaher, Nadin H. Sarg, Nour N. Abu Jayab, Dima W. Alhamad, Taleb H. Al-Tel, Hany A. Omar
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引用次数: 0

摘要

由于肝细胞癌(HCC)对目前的抗癌疗法反应有限,因此需要更有效的治疗方法。能量限制模拟剂(ERMAs)已成为针对沃伯格效应(癌细胞中的一种独特代谢过程)的潜在疗法。然而,ERMAs 在用作单一疗法时疗效有限。此外,ERMAs 还能诱导癌细胞自噬。自噬在癌症生存中的作用仍是一个争论的话题。因此,确定 ERMA 诱导的自噬是 HCC 中细胞存活还是细胞死亡的机制至关重要。我们的研究旨在探讨自噬抑制对接受 ERMAs 治疗的 HCC 细胞存活的影响,同时还研究了将自噬抑制剂(如 spautin-1 )与 ERMAs 结合使用以增强 HCC 细胞死亡的可能性。我们的研究结果表明,ERMA 诱导的自噬在 HCC 细胞中具有细胞保护作用,因为将自噬抑制剂 spautin-1 与 ERMAs 结合使用可有效抑制 ERMA 诱导的自噬,并协同增强其抗肿瘤活性。这种治疗组合通过细胞凋亡、细胞周期停滞和抑制 AKT 和 ERK 的活化促进了 HCC 的死亡,而众所周知,AKT 和 ERK 在细胞增殖中发挥着关键作用。总之,我们的研究结果凸显了通过将能量限制与自噬抑制相结合来抗击 HCC 的潜在策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Autophagy inhibition potentiates energy restriction-induced cell death in hepatocellular carcinoma cells

Hepatocellular carcinoma (HCC) significantly contributes to cancer-related mortality due to the limited response of HCC to current anticancer therapies, thereby necessitating more effective treatment approaches. Energy restriction mimetic agents (ERMAs) have emerged as potential therapies in targeting the Warburg effect, a unique metabolic process in cancer cells. However, ERMAs exhibit limited efficacy when used as monotherapy. Additionally, ERMAs have been found to induce autophagy in cancer cells. The role of autophagy in cancer survival remains a subject of debate. Thus, it is crucial to ascertain whether ERMA-induced autophagy is a mechanism for cell survival or cell death in HCC. Our study aims to investigate the effect of autophagy inhibition on the survival of HCC cells treated with ERMAs while also examining the potential of combining an autophagy inhibitor such as spautin-1 with ERMAs to enhance HCC cell death. Our results suggest a cytoprotective role for ERMA-induced autophagy in HCC cells, as combining the autophagy inhibitor spautin-1 with ERMAs effectively suppressed ERMA-induced autophagy and synergistically enhanced their antitumor activity. The treatment combination promoted HCC death through apoptosis, cell cycle arrest, and inhibition of AKT and ERK activation, which are known to play a key role in cellular proliferation. Collectively, our findings highlight a potential strategy to combat HCC by combining energy restriction with autophagy inhibition.

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来源期刊
IUBMB Life
IUBMB Life 生物-生化与分子生物学
CiteScore
10.60
自引率
0.00%
发文量
109
审稿时长
4-8 weeks
期刊介绍: IUBMB Life is the flagship journal of the International Union of Biochemistry and Molecular Biology and is devoted to the rapid publication of the most novel and significant original research articles, reviews, and hypotheses in the broadly defined fields of biochemistry, molecular biology, cell biology, and molecular medicine.
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