4.3 Article

Propofol-mediated circ_0000735 downregulation restrains tumor growth by decreasing integrin-β1 expression in non-small cell lung cancer

Journal

OPEN MEDICINE
Volume 18, Issue 1, Pages -

Publisher

DE GRUYTER POLAND SP Z O O
DOI: 10.1515/med-2022-0539

Keywords

propofol; NSCLC; circ_0000735; ITGB1

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This study found that propofol can curb the progression of non-small cell lung cancer (NSCLC) by regulating the expression of circ_0000735, reducing cell viability, proliferation, and invasion, and promoting apoptosis. Furthermore, circ_0000735 acts as a sponge for miR-153-3p and regulates the expression of ITGB1, thereby affecting NSCLC. This study provides evidence that propofol inhibits NSCLC progression by regulating circRNA expression.
Propofol, an intravenous anesthetic agent, exerts an anti-tumor peculiarity in multifarious tumors. Circular RNA hsa_circ_0000735 (circ_0000735) is involved in non-small cell lung cancer (NSCLC) progression. The purpose of this study is to investigate whether propofol can curb NSCLC progression via regulating circ_0000735 expression. Cell viability, proliferation, apoptosis, and invasion were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, 5-ethynyl-2 '-deoxyuridine, flow cyto-metry, and transwell assays. Evaluation of protein levels was performed using western blotting or immunohisto-chemistry. Detection of circ_0000735 in tissue samples and cells was carried out using a real-time quantitative poly-merase chain reaction. The molecular mechanisms asso-ciated with circ_0000735 were predicted by bioinformatics analysis and verified by dual-luciferase reporter assays. The relationship between propofol and circ_0000735 in vivo was verified by xenograft models. The results showed that circ_0000735 was overexpressed in NSCLC samples and cells. Propofol treatment overtly decreased circ_0000735 expression in NSCLC cells and repressed NSCLC cell viability, proliferation, invasion, and facilitated NSCLC cell apoptosis, but these effects mediated by propofol were counteracted by circ_0000735 overexpression. Circ_0000735 functioned as a miR-153-3p sponge and regulated integrin-beta 1 (ITGB1) expression via adsorbing miR-153-3p. ITGB1 overexpres-sion reversed circ_0000735 silencing-mediated effects on NSCLC cell viability, proliferation, invasion, and apoptosis. In conclusion, propofol restrained NSCLC growth by down-regulating circ_0000735, which functioned as a miR-153-3p sponge and regulated ITGB1 expression via adsorbing miR-153-3p. This study provides evidence to support that propofol curbs NSCLC progression by regulating circRNA expression.

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