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ATP6V1B1通过mTOR/自噬途径调节卵巢癌进展和顺铂敏感性。

ATP6V1B1 regulates ovarian cancer progression and cisplatin sensitivity through the mTOR/autophagy pathway.

作者信息

Mo Shien, Liu Tingji, Zhou Haiqin, Huang Junning, Zhao Ling, Lu Fangfang, Kuang Yan

机构信息

Department of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.

Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Gaungxi Medical University, Ministry of Education, Nanning, Guangxi, China.

出版信息

Mol Cell Biochem. 2025 Feb;480(2):1013-1026. doi: 10.1007/s11010-024-05025-w. Epub 2024 May 12.

DOI:10.1007/s11010-024-05025-w
PMID:38735913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11835902/
Abstract

Early detection and effective chemotherapy for ovarian cancer, a serious gynecological malignancy, require further progress. This study aimed to investigate the molecular mechanism of ATPase H-Transporting V1 Subunit B1 (ATP6V1B1) in ovarian cancer development and chemoresistance. Our data show that ATP6V1B1 is upregulated in ovarian cancer and correlated with decreased progression-free survival. Gain- and loss-of-function experiments demonstrated that ATP6V1B1 promotes the proliferation, migration, and invasion of ovarian cancer cells in vitro, while ATP6V1B1 knockout inhibits tumor growth in vivo. In addition, knocking down ATP6V1B1 increases the sensitivity of ovarian cancer cells to cisplatin. Mechanistic studies showed that ATP6V1B1 regulates the activation of the mTOR/autophagy pathway. Overall, our study confirmed the oncogenic role of ATP6V1B1 in ovarian cancer and revealed that ATP6V1B1 promotes ovarian cancer progression via the mTOR/autophagy axis.

摘要

对于严重的妇科恶性肿瘤卵巢癌而言，早期检测和有效的化疗仍需进一步进展。本研究旨在探究ATP酶H运输V1亚基B1（ATP6V1B1）在卵巢癌发生发展及化疗耐药中的分子机制。我们的数据表明，ATP6V1B1在卵巢癌中上调，且与无进展生存期缩短相关。功能获得和功能缺失实验表明，ATP6V1B1在体外促进卵巢癌细胞的增殖、迁移和侵袭，而敲除ATP6V1B1在体内抑制肿瘤生长。此外，敲低ATP6V1B1可增加卵巢癌细胞对顺铂的敏感性。机制研究表明，ATP6V1B1调节mTOR/自噬通路的激活。总体而言，我们的研究证实了ATP6V1B1在卵巢癌中的致癌作用，并揭示ATP6V1B1通过mTOR/自噬轴促进卵巢癌进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/ce9c9f05a490/11010_2024_5025_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/b7c8a0be7586/11010_2024_5025_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/42cd495a07ff/11010_2024_5025_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/c9872f94b731/11010_2024_5025_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/dbf89d363ba6/11010_2024_5025_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/32dd50ee9fac/11010_2024_5025_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/ce9c9f05a490/11010_2024_5025_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/b7c8a0be7586/11010_2024_5025_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/42cd495a07ff/11010_2024_5025_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/c9872f94b731/11010_2024_5025_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/dbf89d363ba6/11010_2024_5025_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/32dd50ee9fac/11010_2024_5025_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be66/11835902/ce9c9f05a490/11010_2024_5025_Fig6_HTML.jpg

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