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Article

Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway

  • Authors:
    • Suolin Zhang
    • Yayan Wang
  • View Affiliations / Copyright

    Affiliations: Department of Chest Surgery, The Second Hospital of Shandong University, Jinan, Shandong 250000, P.R. China, Department of Respiratory Medicine, Affiliated Hospital of Yanbian University, Yanji, Jilin 133000, P.R. China
  • Pages: 5859-5864
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    Published online on: February 8, 2018
       https://doi.org/10.3892/ol.2018.8002
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Abstract

Expression of angiotensin II (Ang II), a key biological peptide in the renin‑angiotensin system, is closely associated with the occurrence and development of cancer. Ang II binds two receptor subtypes, the Ang II type 1 receptor (AT1R) and the AT2R, to mediate a series of biological effects. Telmisartan, a specific AT1R blocker, has been reported to have potential as an anticancer drug for treating renal cancer. In the present study, whether telmisartan had an effect on non‑small cell lung cancer (NSCLC) cell proliferation and migration was investigated. The Cell Counting kit‑8 assay revealed that telmisartan significantly inhibited the growth of the NSCLC A549 cell line in a time‑ and dose‑dependent manner. In a transwell assay, telmisartan significantly inhibited cellular invasion and migration. Furthermore, it was determined that the expression of the anti‑apoptotic protein B‑cell lymphoma was decreased, and that of the pro‑apoptotic proteins caspase‑3 and Bcl‑associated X increased in the A549 cells treated with telmisartan. Additionally, levels of phosphorylated RAC serine/threonine‑protein kinase (p‑AKT), p‑mechanistic target of rapamycin, p70‑S6 kinase and cyclin D1 was decreased in the telmisartan‑treated group. Therefore, the current study reveals that telmisartan‑induced NSCLC apoptosis may be regulated via the phosphoinositide 3‑kinase/AKT signaling pathway, which indicates that it may be a potential novel drug for clinical NSCLC treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang S and Wang Y: Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway. Oncol Lett 15: 5859-5864, 2018.
APA
Zhang, S., & Wang, Y. (2018). Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway. Oncology Letters, 15, 5859-5864. https://doi.org/10.3892/ol.2018.8002
MLA
Zhang, S., Wang, Y."Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway". Oncology Letters 15.4 (2018): 5859-5864.
Chicago
Zhang, S., Wang, Y."Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway". Oncology Letters 15, no. 4 (2018): 5859-5864. https://doi.org/10.3892/ol.2018.8002
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang S and Wang Y: Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway. Oncol Lett 15: 5859-5864, 2018.
APA
Zhang, S., & Wang, Y. (2018). Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway. Oncology Letters, 15, 5859-5864. https://doi.org/10.3892/ol.2018.8002
MLA
Zhang, S., Wang, Y."Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway". Oncology Letters 15.4 (2018): 5859-5864.
Chicago
Zhang, S., Wang, Y."Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway". Oncology Letters 15, no. 4 (2018): 5859-5864. https://doi.org/10.3892/ol.2018.8002
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