In:
International Journal of Toxicology, SAGE Publications, Vol. 41, No. 3 ( 2022-05), p. 212-224
Kurzfassung:
The aim of this study was to investigate the mechanism of isoflurane in proliferation, invasion, and migration in prostate cancer (PC) cells in vitro by regulating BACH1 and miR-375. The effect of different concentrations of isoflurane (0%, 0.5%, 1%, and 2%) on PC cell proliferation (PC3 and 22RV1) was measured. After PC cells and normal human prostate stromal immortalized WPMY-1 cells were treated with isoflurane, BACH1 and miR-375 expression was measured. Subsequently, PC3 and 22RV1 cells underwent gain- and loss-of-function assays with or without 4-h 2% isoflurane pretreatment. The levels of miR-375, BACH1, and PTEN were assessed. The binding of BACH1 to miR-375 promoter was detected by ChIP assay. Dual-luciferase reporter assay detected the targeting relationship of miR-375 with BACH1 and PTEN. Isoflurane promoted PC3 and 22RV1 cell proliferation. In addition, isoflurane elevated the levels of BACH1 and miR-375 in a dosage-dependent manner in PC cells. Transfection with miR-375 inhibitor or sh-BACH1 repressed PC cell proliferation, invasion, and migration, while exposure to 2% isoflurane for 4 h before transfection counteracted the inhibitory effects of sh-BACH1 or miR-375 inhibitor on PC cells. PTEN expression was suppressed after 2% isoflurane treatment, but the transfection with miR-375 inhibitor partly abrogated this suppressive effect in PC cells. Moreover, BACH1 bound to miR-375 and miR-375 negatively targeted PTEN. miR-375 mimic could partially reverse the inhibitory effects of sh-BACH1 on the proliferation, invasion, and migration of isoflurane-treated PC cells. Isoflurane facilitated PC cell proliferation, migration, and invasion by activating BACH1 to upregulate miR-375.
Materialart:
Online-Ressource
ISSN:
1091-5818
,
1092-874X
DOI:
10.1177/10915818221084906
Sprache:
Englisch
Verlag:
SAGE Publications
Publikationsdatum:
2022
ZDB Id:
1500682-7
