CXCL1 gene silencing inhibits HGC803 cell migration and invasion and acts as an independent prognostic factor for poor survival in gastric cancer

نویسندگان

  • Liang Wang
  • Changhua Zhang
  • Jianbo Xu
  • Hui Wu
  • Jianjun Peng
  • Shirong Cai
  • Yulong He
چکیده

Chemokine (C-X-C motif) ligand 1 (CXCL1) is essential in oncogenesis and development of malignant tumors. The present study aimed to investigate CXCL1 expression in promoting lymph node metastasis in gastric cancer patients. Human gastric cancer cell lines were employed to detect CXCL1 expression. HGC803 cell migration and cell invasion were detected using a wound healing assay and Transwell invasion assay, respectively. A total of 100 patients who underwent radical gastric resection with lymph node dissection in the First Affiliated Hospital of Sun Yat‑Sen University (Guangzhou, China) between 2007 and 2008 were included. Expression of CXCL1 and lymphatic vessel density (LMVD) was determined by using immunohistochemistry (IHC), and their association with clinicopathological features and prognosis was investigated. Cox survival regression analysis was used to analyze overall survival of patients. Results indicated that CXCL1 protein was expressed in all of investigated gastric cancer cell lines. Silencing of the CXCL1 gene reduced migratory and invasive ability of HGC803 cells. CXCL1 protein expression was detected by IHC in 41 patients (41%), these were associated with advanced tumor‑node‑metastasis (TNM) stage, LMVD, tumor differentiation and poor survival. LMVD was positively correlated with advanced TNM stage, size of tumor, tumor differentiation and poor survival rate. Furthermore, it was observed that TNM stage, tumor differentiation and CXCL1 were independent prognostic factors in the Cox survival regression analysis. Silencing of the CXCL1 gene inhibits HGC803 cell migration and invasion. The positive expression of CXCL1 is correlated with poor survival of gastric cancer patients and CXCL1 is an independent prognostic factor for gastric cancer.

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عنوان ژورنال:

دوره 14  شماره 

صفحات  -

تاریخ انتشار 2016