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Article

HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27

  • Authors:
    • Zefei Wang
    • Chunzhi Yu
    • Hong Wang
  • View Affiliations / Copyright

    Affiliations: Department of Gynecology and Obstetrics, The Fourth People's Hospital of Shaanxi, Xi'an, Shaanxi 710000, P.R. China, Department of Obstetrics, The Northwest Women's and Children's Hospital, Xi'an, Shaanxi 710000, P.R. China, Department of Oncology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China
  • Pages: 1122-1130
    |
    Published online on: November 20, 2018
       https://doi.org/10.3892/or.2018.6874
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Abstract

Homeobox A5 (HOXA5) is a member of the homeobox gene (HOX) family, which plays an important role in the development of various malignant tumors. Here, we speculated that HOXA5 has an effect on cervical cancer development. In our study, we aimed to explore the role and molecular mechanism of HOXA5 in regards to the cell proliferation and apoptosis in cervical cancer. We found that expression levels of HOXA5 measured by RT‑qPCR and western blot assays in cervical cancer cell lines and tissues were both significantly downregulated. We performed a gain‑of‑function experiment by the transfection with pcDNA.3.1‑HOXA5 in ME‑180 and HT‑3 cells to overexpress HOXA5, and the caspase‑3 activity measured by caspase‑3 activity assay kit and cell apoptosis detected by flow cytometry were obviously promoted. Meanwhile, cell proliferation tested by BrdU assay, invasion determined by Transwell and cell viability tested by MTT were inhibited. Moreover, protein kinase B (AKT) was activated by incubation with SC79 (AKT activator; 1 µg/ml) after HOXA5 overexpression, and reversed the effect of HOXA5 overexpression on p27 expression. Additionally, significant elevation of AKT activation measured by western blot analysis abrogated the effect of HOXA5 on caspase‑3 activity, cell apoptosis, proliferation, invasion and cell viability. Taken together, this study revealed that HOXA5 inhibits cervical cancer progression by regulating AKT/p27, proposing the potential role of HOXA5 in the prevention and treatment of cervical cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Wang Z, Yu C and Wang H: HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27. Oncol Rep 41: 1122-1130, 2019.
APA
Wang, Z., Yu, C., & Wang, H. (2019). HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27. Oncology Reports, 41, 1122-1130. https://doi.org/10.3892/or.2018.6874
MLA
Wang, Z., Yu, C., Wang, H."HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27". Oncology Reports 41.2 (2019): 1122-1130.
Chicago
Wang, Z., Yu, C., Wang, H."HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27". Oncology Reports 41, no. 2 (2019): 1122-1130. https://doi.org/10.3892/or.2018.6874
Copy and paste a formatted citation
x
Spandidos Publications style
Wang Z, Yu C and Wang H: HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27. Oncol Rep 41: 1122-1130, 2019.
APA
Wang, Z., Yu, C., & Wang, H. (2019). HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27. Oncology Reports, 41, 1122-1130. https://doi.org/10.3892/or.2018.6874
MLA
Wang, Z., Yu, C., Wang, H."HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27". Oncology Reports 41.2 (2019): 1122-1130.
Chicago
Wang, Z., Yu, C., Wang, H."HOXA5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase B and p27". Oncology Reports 41, no. 2 (2019): 1122-1130. https://doi.org/10.3892/or.2018.6874
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