MAFG-AS1在卵巢癌中的过表达通过调节HIF-1α促进卵巢癌细胞的糖代谢重编程和恶性生物学行为。

Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α.

作者信息

Jia Liu, Yu Fei

机构信息

Department of Pathology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No.88 Jiefang, Hangzhou, 310009, Zhejiang, China.

出版信息

Discov Oncol. 2025 May 15;16(1):769. doi: 10.1007/s12672-025-02429-y.

DOI:10.1007/s12672-025-02429-y

PMID:40372661

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12081788/

Abstract

OBJECTIVE

This research explored the involvement of MAFG-AS1 in metabolic reprogramming and potential molecular mechanisms in ovarian cancer (OC).

METHODS

The ability of MAFG-AS1 silencing to affect the glucose intake, lactate production, ECAR, OCR and ATP concentrations and NAD/NADH ratios in OC cells was examined. Cell cycle phases and apoptosis were measured by flow cytometry. The influences of MAFG-AS1overexprssion on the above assays were also identified.

RESULTS

A transient reduction in the number of SKOV3 and HO8910 cells in the MAFG-AS1 knockdown group. MAFG-AS1 knockdown can inhibit cell proliferation, induce apoptosis, and enhance the number of cells in G2 phase. Silencing MAFG-AS1 can inhibit the glucose uptake rate, extracellular lactate production, and ECAR of OC cells, ATP levels, and can promote OCR and NAD/ NADH ratio oxidative phosphorylation. Silencing MAFG-AS1 can inhibit HIF-1α in OC.

CONCLUSION

Our study revealed silencing MAFG-AS1 could inhibit the proliferation and induce apoptosis of OC cells by inhibiting the HIF-1α-mediated glycolysis process. Therefore, this study further potentially reveals the machinery of MAFG-AS1 in regulating OC cell proliferation and apoptosis, which is expected to provide a theoretical basis for the study of new targets.

摘要

目的

本研究探讨了MAFG-AS1在卵巢癌（OC）代谢重编程中的作用及潜在分子机制。

方法

检测MAFG-AS1沉默对OC细胞葡萄糖摄取、乳酸生成、细胞外酸化率（ECAR）、氧消耗率（OCR）、ATP浓度及NAD/NADH比值的影响。通过流式细胞术检测细胞周期阶段和细胞凋亡情况。还确定了MAFG-AS1过表达对上述检测的影响。

结果

MAFG-AS1敲低组中SKOV3和HO8910细胞数量短暂减少。MAFG-AS1敲低可抑制细胞增殖、诱导细胞凋亡，并增加G2期细胞数量。沉默MAFG-AS1可抑制OC细胞的葡萄糖摄取率、细胞外乳酸生成及ECAR、ATP水平，并可促进OCR及NAD/NADH比值的氧化磷酸化。沉默MAFG-AS1可抑制OC中的缺氧诱导因子-1α（HIF-1α）。