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

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

doi:10.1007/s11010-024-05025-w

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

Mol Cell Biochem. 2024 May 12. doi: 10.1007/s11010-024-05025-w. Online ahead of print.

Authors

Shien Mo^#^{1

2

3}, Tingji Liu^#¹, Haiqin Zhou^#^{1

2

3}, Junning Huang¹, Ling Zhao¹, Fangfang Lu¹, Yan Kuang^{4

5

6}

Affiliations

¹ Department of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
² Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Gaungxi Medical University, Ministry of Education, Nanning, Guangxi, China.
³ Guangxi Key Laboratory of High-Incidence-Tumor Prevention & Treatment, Guangxi Medical University, Nanning, Guangxi, China.
⁴ Department of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China. kuangyan_2004@163.com.
⁵ Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Gaungxi Medical University, Ministry of Education, Nanning, Guangxi, China. kuangyan_2004@163.com.
⁶ Guangxi Key Laboratory of High-Incidence-Tumor Prevention & Treatment, Guangxi Medical University, Nanning, Guangxi, China. kuangyan_2004@163.com.

^# Contributed equally.

PMID: 38735913
DOI: 10.1007/s11010-024-05025-w

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.

Keywords: ATP6V1B1; Autophagy; Cisplatin sensitivity; Ovarian cancer; V-ATPase; mTOR.

Abstract

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