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Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma

  • Authors:
    • Chao Tang
    • Jin Wang
    • Qi Wei
    • Yi‑Peng Du
    • He‑Ping Qiu
    • Chao Yang
    • Yu‑Chuan Hou
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, Department of Anesthesiology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
    Copyright: © Tang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 7060-7068
    |
    Published online on: March 7, 2018
       https://doi.org/10.3892/ol.2018.8204
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Abstract

Tropomyosin-1 (TPM1), a widely expressed actin‑binding protein, is downregulated in many tumors and associated with cancer progression. A previous study from our group suggested that TPM1 could be involved in renal cell carcinoma (RCC) apoptosis, but the mechanisms and details remained unknown. The present study aimed to further examine the proapoptotic effects of TPM1 and investigate the underlying mechanisms in RCC cell lines. Results from cell viability, DAPI staining and apoptosis assays demonstrated that TPM1 upregulation inhibited cell proliferation and promoted cell apoptosis in both 786‑O and ACHN RCC cell lines. However, TPM1 knockdown in the two RCC cell lines did not result in the opposite effects on cell proliferation or cell apoptosis. Comet assay and western blotting results demonstrated that TPM1 overexpression induced DNA damage and decreased the expression levels of the antiapoptotic factor BCL2 apoptosis regulator, while increasing the expression levels of the proapoptotic factors BCL2 associated X, Caspase‑3 and p53 in 786‑O and ACHN cells. The present findings suggest that TPM1 overexpression in RCC cell lines can induce tumor cell apoptosis via the p53‑mediated mitochondrial pathway. Further studies are needed to fully elucidate the potential of TPM1 as a candidate for RCC targeted therapy in the future.
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Copy and paste a formatted citation
Spandidos Publications style
Tang C, Wang J, Wei Q, Du YP, Qiu HP, Yang C and Hou YC: Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma. Oncol Lett 15: 7060-7068, 2018.
APA
Tang, C., Wang, J., Wei, Q., Du, Y., Qiu, H., Yang, C., & Hou, Y. (2018). Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma. Oncology Letters, 15, 7060-7068. https://doi.org/10.3892/ol.2018.8204
MLA
Tang, C., Wang, J., Wei, Q., Du, Y., Qiu, H., Yang, C., Hou, Y."Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma". Oncology Letters 15.5 (2018): 7060-7068.
Chicago
Tang, C., Wang, J., Wei, Q., Du, Y., Qiu, H., Yang, C., Hou, Y."Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma". Oncology Letters 15, no. 5 (2018): 7060-7068. https://doi.org/10.3892/ol.2018.8204
Copy and paste a formatted citation
x
Spandidos Publications style
Tang C, Wang J, Wei Q, Du YP, Qiu HP, Yang C and Hou YC: Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma. Oncol Lett 15: 7060-7068, 2018.
APA
Tang, C., Wang, J., Wei, Q., Du, Y., Qiu, H., Yang, C., & Hou, Y. (2018). Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma. Oncology Letters, 15, 7060-7068. https://doi.org/10.3892/ol.2018.8204
MLA
Tang, C., Wang, J., Wei, Q., Du, Y., Qiu, H., Yang, C., Hou, Y."Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma". Oncology Letters 15.5 (2018): 7060-7068.
Chicago
Tang, C., Wang, J., Wei, Q., Du, Y., Qiu, H., Yang, C., Hou, Y."Tropomyosin-1 promotes cancer cell apoptosis via the p53-mediated mitochondrial pathway in renal cell carcinoma". Oncology Letters 15, no. 5 (2018): 7060-7068. https://doi.org/10.3892/ol.2018.8204
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