Rapamycin suppresses the PI3K/AKT/mTOR signaling pathway by targeting SIRT1 in esophageal cancer
- Tao Liu
- Xiangsen Liang
- Yu Sun
- Shengzhuang Yang
Affiliations: Department of Cardiothoracic Surgery, Guangxi International Zhuang Medical Hospital, Nanning, Guangxi 530201, P.R. China, Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, P.R. China
- Published online on: August 17, 2021 https://doi.org/10.3892/etm.2021.10624
Copyright: © Liu
et al. This is an open access article distributed under the
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Rapamycin, a secondary metabolite produced by Streptomyces hygroscopicus, is known for its pharmacological effects, especially antitumor and immunosuppressive activities. However, the antitumoral effects of rapamycin in human esophageal cancer (EC) are still poorly understood. To investigate the potential of rapamycin in EC treatment, sirtuin 1 (SIRT1) mRNA expression was quantified in the tissue of patients with EC or in EC cell lines using reverse transcription‑quantitative PCR. The protein levels of SIRT1 and PI3K/AKT/mTOR were measured via western blotting. Furthermore, cell viability, migration and invasion were investigated by Cell Counting Kit‑8, wound healing and Transwell assays, respectively. The present results suggested that SIRT1 expression was upregulated in EC. In vitro, the inhibitory effect of rapamycin on cell viability in EC was strengthened or weakened after small interfering (si)‑SIRT1 or pcDNA3.1/SIRT1 transfection. Furthermore, SIRT1 rescued the inhibitory effect of rapamycin on the migration and invasion of EC cells. In vivo, si‑SIRT1 or SIRT1 overexpression in mice could enhance or rescue the inhibitory effects of rapamycin on tumor growth. In addition, SIRT1 transfection rescued the decreased level of phosphorylated (p)‑PI3K, p‑AKT and p‑mTOR induced by rapamycin treatment. Taken together, the present results suggested that rapamycin suppressed the cell viability, migration, invasion and PI3K/AKT/mTOR signaling pathway in EC by negatively regulating SIRT1.