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Article

CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells

  • Authors:
    • Qian Guo
    • Zhixiang Jian
    • Baoqing Jia
    • Liang Chang
  • View Affiliations / Copyright

    Affiliations: Graduate College, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of Breast Neoplasms Surgery, People's Hospital of Inner Mongolia, Hohhot, Inner Mongolia 010017, P.R. China, Department of Oncology Surgery, Inner Mongolia Baogang Hospital, Baotou, Inner Mongolia 404010, P.R. China
  • Pages: 1114-1122
    |
    Published online on: December 12, 2016
       https://doi.org/10.3892/or.2016.5312
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Abstract

CXCL7 is an important chemoattractant cytokine, which signals through binding to its receptor CXCR2. Recent studies have demonstrated that the CXCL7/CXCR2 signaling plays a promoting role in several common malignancies, including lung, renal, colon, and breast cancer. However, the regulatory role of CXCL7, in cholangiocarcinoma, as well as the underlying mechanism, has not been previously reported. Herein, we found more positive expression of CXCL7 in cholangiocarcinoma tissues compared to adjacent non-tumor tissues. High CXCL7 expression was significantly correlated with poor differentiation, lymph node metastasis, vascular invasion and advanced clinical stage, but was not associated with age, gender, or tumor size. Besides, the expression of CXCL7 was significantly associated with the Ki67 expression, but not associated with CA199, AFP, or P53 expression in cholangiocarcinoma. Moreover, the overall survival of cholangiocarcinoma patients with high CXCL7 expression was significantly shorter than those with low CXCL7 expression. In vitro study indicated that CXCL7 and CXCR2 were also positively expressed in several common cholangiocarcinoma cell lines, including HuCCT1, HuH28, QBC939, EGI-1, OZ and WITT. SiRNA-induced inhibition of CXCL7 significantly reduced the proliferation and invasion of QBC939 cells. On the contrary, overexpression of CXCL7 markedly promoted these malignant phenotypes of QBC939 cells. Of note, the conditioned medium of CXCL7-overexpresing human hepatic stellate cells could also promote the proliferation and invasion of QBC939 cells, suggesting that CXCL7 may also play an oncogenic role in cholangiocarcinoma in a paracrine-dependent manner, not only in an autocrine-dependent manner. Molecular assay data suggested that the AKT signaling pathway was involved in the CXCL7-mediated malignant phenotypes of QBC939 cells. In summary, our study suggests that CXCL7 plays a promoting role in regulating the growth and metastasis of cholangiocarcinoma.
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Copy and paste a formatted citation
Spandidos Publications style
Guo Q, Jian Z, Jia B and Chang L: CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells. Oncol Rep 37: 1114-1122, 2017.
APA
Guo, Q., Jian, Z., Jia, B., & Chang, L. (2017). CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells. Oncology Reports, 37, 1114-1122. https://doi.org/10.3892/or.2016.5312
MLA
Guo, Q., Jian, Z., Jia, B., Chang, L."CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells". Oncology Reports 37.2 (2017): 1114-1122.
Chicago
Guo, Q., Jian, Z., Jia, B., Chang, L."CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells". Oncology Reports 37, no. 2 (2017): 1114-1122. https://doi.org/10.3892/or.2016.5312
Copy and paste a formatted citation
x
Spandidos Publications style
Guo Q, Jian Z, Jia B and Chang L: CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells. Oncol Rep 37: 1114-1122, 2017.
APA
Guo, Q., Jian, Z., Jia, B., & Chang, L. (2017). CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells. Oncology Reports, 37, 1114-1122. https://doi.org/10.3892/or.2016.5312
MLA
Guo, Q., Jian, Z., Jia, B., Chang, L."CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells". Oncology Reports 37.2 (2017): 1114-1122.
Chicago
Guo, Q., Jian, Z., Jia, B., Chang, L."CXCL7 promotes proliferation and invasion of cholangiocarcinoma cells". Oncology Reports 37, no. 2 (2017): 1114-1122. https://doi.org/10.3892/or.2016.5312
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