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Article

KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance

  • Authors:
    • Tongfu Feng
    • Yan Wang
    • Yan Lang
    • Yuanzhen Zhang
  • View Affiliations / Copyright

    Affiliations: Center of Reproductive Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China, Department of Gynecology, Hubei Maternal and Children's Hospital, Wuhan, Hubei 430070, P.R. China
  • Pages: 3573-3580
    |
    Published online on: July 12, 2017
       https://doi.org/10.3892/mmr.2017.6960
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Abstract

The authors initially performed reverse transcription‑quantitative polymerase chain reaction to determine the expression profile of KDM5A in ovarian cancer tissues and adjacent normal tissue. Compared with adjacent normal tissue, it was identified that KDM5A was highly expressed in ovarian cancer tissues. Moreover, human ovarian cell lines also confirmed that KDM5A was highly expressed in ovarian cancer. KDM5A was especially highly expressed in SKOV3/paclitaxel (PTX) cells, which are resistant to PTX. Previous studies demonstrated that chemoresistance in cancer cells facilitates epithelial‑to‑mesenchymal transition (EMT). Following this, whether KDM5A influenced EMT and metastasis was investigated. The expression of KDM5A and N‑cadherin were obviously higher in SKOV3/PTX cells than in SKOV3 cells. The expression of E‑cadherin was decreased and the expression of N‑cadherin was increased following ectopic expression of KDM5A, while the expression of E‑cadherin was increased and the expression of N‑cadherin was decreased following KDM5A depletion. Transwell and wound healing assays were used to explore the function of KMD5A in metastasis. The present results indicated that KDM5A facilitated EMT and metastasis in ovarian cells. Moreover, it was identified that P‑glycoprotein was increased while KDM5A was expressed ectopically in SKOV3 cells. Following fluorescence‑activated cell sorting flow cytometry analysis and CCK‑8 assay all revealed that KDM5A regulated the PTX sensitivity in SKOV3 and SKOV3/PTX cells. In brief, KDM5A is a crucial oncogene that is significantly upregulated in ovarian cancer. Its expression is closely correlated with cancer cell proliferation, EMT and metastasis. KDM5A suppresses ovarian cancer cell apoptosis under PTX treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Feng T, Wang Y, Lang Y and Zhang Y: KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance. Mol Med Rep 16: 3573-3580, 2017.
APA
Feng, T., Wang, Y., Lang, Y., & Zhang, Y. (2017). KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance. Molecular Medicine Reports, 16, 3573-3580. https://doi.org/10.3892/mmr.2017.6960
MLA
Feng, T., Wang, Y., Lang, Y., Zhang, Y."KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance". Molecular Medicine Reports 16.3 (2017): 3573-3580.
Chicago
Feng, T., Wang, Y., Lang, Y., Zhang, Y."KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance". Molecular Medicine Reports 16, no. 3 (2017): 3573-3580. https://doi.org/10.3892/mmr.2017.6960
Copy and paste a formatted citation
x
Spandidos Publications style
Feng T, Wang Y, Lang Y and Zhang Y: KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance. Mol Med Rep 16: 3573-3580, 2017.
APA
Feng, T., Wang, Y., Lang, Y., & Zhang, Y. (2017). KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance. Molecular Medicine Reports, 16, 3573-3580. https://doi.org/10.3892/mmr.2017.6960
MLA
Feng, T., Wang, Y., Lang, Y., Zhang, Y."KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance". Molecular Medicine Reports 16.3 (2017): 3573-3580.
Chicago
Feng, T., Wang, Y., Lang, Y., Zhang, Y."KDM5A promotes proliferation and EMT in ovarian cancer and closely correlates with PTX resistance". Molecular Medicine Reports 16, no. 3 (2017): 3573-3580. https://doi.org/10.3892/mmr.2017.6960
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