ATP6V1B1 regulates ovarian cancer progression and cisplatin sensitivity through the mTOR/autophagy pathway
View abstract on PubMed
Summary
This summary is machine-generated.ATPase H<sup>+</sup>-Transporting V1 Subunit B1 (ATP6V1B1) drives ovarian cancer progression and chemoresistance by regulating the mTOR/autophagy pathway. Targeting ATP6V1B1 may offer new therapeutic strategies for ovarian cancer patients.
Area Of Science
- Gynecological Oncology
- Molecular Biology
- Cancer Research
Background
- Ovarian cancer remains a significant gynecological malignancy with unmet needs in early detection and chemotherapy.
- Understanding the molecular drivers of ovarian cancer progression and chemoresistance is crucial for developing effective treatments.
Purpose Of The Study
- To investigate the role of ATPase H<sup>+</sup>-Transporting V1 Subunit B1 (ATP6V1B1) in ovarian cancer development.
- To elucidate the molecular mechanism by which ATP6V1B1 influences ovarian cancer cell proliferation, migration, invasion, and chemoresistance.
Main Methods
- Analysis of ATP6V1B1 expression in ovarian cancer tissues.
- In vitro gain- and loss-of-function experiments (including ATP6V1B1 knockout).
- In vivo tumor growth studies.
- Investigation of the mTOR/autophagy pathway activation.
Main Results
- ATP6V1B1 is upregulated in ovarian cancer and associated with reduced progression-free survival.
- ATP6V1B1 overexpression promotes ovarian cancer cell proliferation, migration, and invasion in vitro.
- ATP6V1B1 knockout inhibits tumor growth in vivo.
- Reduced ATP6V1B1 levels enhance sensitivity to cisplatin chemotherapy.
- ATP6V1B1 regulates the activation of the mTOR/autophagy pathway.
Conclusions
- ATP6V1B1 acts as an oncogene in ovarian cancer.
- ATP6V1B1 promotes ovarian cancer progression and chemoresistance through the mTOR/autophagy signaling axis.
- ATP6V1B1 represents a potential therapeutic target for ovarian cancer.
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