Hyperthermia, as an anticancer therapeutic strategy, presents notable advantages in conjunction with irradiation and/or chemotherapy in the treatment of cancer by promoting apoptosis and inhibiting proliferation. A number of studies have documented that hyperthermia inhibits cancer progression through transcriptional activation of p53, which promotes cell cycle arrest and apoptosis. However, the underlying molecular mechanisms of hyperthermia-regulated apoptosis and proliferation dependent on p53 remain largely unknown. To investigate the effects and molecular mechanism of hyperthermia on the apoptosis and proliferation of colorectal carcinoma (CRC) HCT116 cells, the present study assessed cell apoptosis and proliferation following exposure to hyperthermia (42°C for 2–4 h). The results indicated that, compared with the control group at 0 h, hyperthermia exposure for 2 and 4 h induced the apoptosis of HCT116 cells (P<0.05), inhibited cell proliferation by causing cell cycle arrest at G1/G0 phase (P<0.05), and significantly increased microRNA (miR)-34a expression (P<0.05), but not miR-34b, miR-34c, miR-215 and miR-504 expression. The transcriptional activity of p53 on its consensus sequence and downstream target genes, namely p21, B cell lymphoma 2-associated X protein, mouse double minute 2 homolog, p53 upregulated modulator of apoptosis and growth arrest and DNA-damage-inducible 45α, was subsequently detected. The data indicated significantly higher transcriptional activity of p53 following hyperthermia exposure for 2 and 4 h (P<0.05), and these observations were similar to the effects of transfection with miR-34a mimics in HCT116 cells. Furthermore, transfection with miR-34a antagomiR supressed hyperthermia-induced apoptosis and promoted cell cycle progression following hyperthermia exposure when compared with transfection controls (P<0.05). Collectively, these findings indicate that miR-34a may serve an important role in hyperthermia-regulated apoptosis and proliferation in HCT116 cells by influencing the transcriptional activity of p53.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.