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Isoflurane Promotes Cell Proliferation, Invasion, and Migration by Regulating BACH1 and miR-375 in Prostate Cancer
Jue Zheng1, Guiheng Chen1, Tieqiu Li1
1Department of Urology, 87803Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, P.R. China.
International Journal of Toxicology
|May 9, 2022
Summary
Isoflurane promotes prostate cancer (PC) cell growth by increasing BACH1 and miR-375. Inhibiting these factors reduces PC cell proliferation, invasion, and migration, suggesting a therapeutic target.
Area of Science:
- Oncology
- Anesthesiology
- Molecular Biology
Background:
- Prostate cancer (PC) remains a significant health concern, with limited therapeutic options for advanced stages.
- Understanding the molecular mechanisms driving PC progression, including proliferation, invasion, and migration, is crucial for developing effective treatments.
- Isoflurane, a common anesthetic, has shown potential in influencing cancer cell behavior, necessitating further investigation into its specific molecular targets.
Purpose of the Study:
- To elucidate the in vitro mechanism by which isoflurane affects prostate cancer cell proliferation, invasion, and migration.
- To investigate the roles of BACH1 and miR-375 as key regulators in isoflurane-mediated effects on PC cells.
- To determine the regulatory relationship between isoflurane, BACH1, miR-375, and PTEN in prostate cancer.
Main Methods:
- Prostate cancer cell lines (PC3 and 22RV1) were treated with varying concentrations of isoflurane.
- Expression levels of BACH1 and miR-375 were measured using quantitative assays.
- Gain- and loss-of-function experiments were performed, including transfections with miR-375 inhibitors and sh-BACH1, alongside isoflurane treatment.
- Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were utilized to confirm molecular interactions.
Main Results:
- Isoflurane significantly promoted proliferation, invasion, and migration of PC3 and 22RV1 cells in a dose-dependent manner.
- Isoflurane treatment led to increased expression of both BACH1 and miR-375 in PC cells.
- Inhibition of BACH1 or miR-375 suppressed PC cell progression, an effect counteracted by isoflurane pre-treatment.
- Isoflurane downregulated PTEN expression, partially mediated by miR-375, and BACH1 was found to bind to the miR-375 promoter.
Conclusions:
- Isoflurane facilitates prostate cancer cell proliferation, migration, and invasion through the activation of BACH1, leading to the upregulation of miR-375.
- The study identifies a novel regulatory pathway involving isoflurane, BACH1, miR-375, and PTEN in prostate cancer progression.
- Targeting the BACH1-miR-375 axis presents a potential therapeutic strategy for managing isoflurane-influenced prostate cancer.
