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Article

Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A

  • Authors:
    • Chun-Mei Yan
    • Ying-Ling Zhao
    • Hong-Yi Cai
    • Guo-Ying Miao
    • Wen Ma
  • View Affiliations / Copyright

    Affiliations: Lanzhou Jiao Tong University Hospital, Lanzhou 730000, P.R. China, Department of Hematology, Gansu Provincial Hospital, Lanzhou 730000, P.R. China, Department of Radiotherapy Oncology, Gansu Provincial Hospital, Lanzhou 730000, P.R. China
  • Pages: 1737-1744
    |
    Published online on: January 29, 2015
       https://doi.org/10.3892/or.2015.3769
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Abstract

Gene therapy is a promising therapeutic approach for chemoresistant cervical cancers. Therapeutic interventions targeting the key factors contributing to the initiation and progression of cervical cancer may be a more effective treatment strategy. In the present study, we firstly determined the expression of protein tyrosine phosphatase receptor J (PTPRJ) in 8-paired human cervical tumor and non-tumor tissues. We observed a striking downregulation of PTPRJ in the human cervical tumor tissues. Next, we investigated the roles and the function mechanism of PTPRJ in the human cervical carcinoma cell line C33A by loss- and gain-of-function experiments. Our study indicated that C33A cells with loss of PTPRJ expression showed a significantly increased cell viability, rising growth and migration rate, as well as a G1-S transition. We obtained the opposite results when we overexpressed PTPRJ in C33A cells. Our further study indicated that PTPRJ levels were highly correlated with cell survival when the C33A cells were treated with 5-fluorouracil (5-FU), an important chemotherapeutic agent for cervical cancer. In addition, the signaling pathway screening assay showed an obvious alteration of the Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) pathway. PTPRJ negatively regulated the activation of the JAK1/STAT3 pathway by decreasing the phosphorylation levels of JAK1 and STAT3. In addition, PTPRJ also regulated the expression of the downstream factors of STAT3, such as cyclin D, Bax, VEGF and MMP2. Our results suggest that PTPRJ may be a promising gene therapy target and its therapeutic potential can be fulfilled when used alone, or in combination with other anticancer agents.
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Copy and paste a formatted citation
Spandidos Publications style
Yan C, Zhao Y, Cai H, Miao G and Ma W: Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A. Oncol Rep 33: 1737-1744, 2015.
APA
Yan, C., Zhao, Y., Cai, H., Miao, G., & Ma, W. (2015). Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A. Oncology Reports, 33, 1737-1744. https://doi.org/10.3892/or.2015.3769
MLA
Yan, C., Zhao, Y., Cai, H., Miao, G., Ma, W."Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A". Oncology Reports 33.4 (2015): 1737-1744.
Chicago
Yan, C., Zhao, Y., Cai, H., Miao, G., Ma, W."Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A". Oncology Reports 33, no. 4 (2015): 1737-1744. https://doi.org/10.3892/or.2015.3769
Copy and paste a formatted citation
x
Spandidos Publications style
Yan C, Zhao Y, Cai H, Miao G and Ma W: Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A. Oncol Rep 33: 1737-1744, 2015.
APA
Yan, C., Zhao, Y., Cai, H., Miao, G., & Ma, W. (2015). Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A. Oncology Reports, 33, 1737-1744. https://doi.org/10.3892/or.2015.3769
MLA
Yan, C., Zhao, Y., Cai, H., Miao, G., Ma, W."Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A". Oncology Reports 33.4 (2015): 1737-1744.
Chicago
Yan, C., Zhao, Y., Cai, H., Miao, G., Ma, W."Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A". Oncology Reports 33, no. 4 (2015): 1737-1744. https://doi.org/10.3892/or.2015.3769
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