科研之友
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摘要
Objective To investigate the expression of CXC chemokine ligand 11 (CXCL11) in gallbladder cancer (GBC) and its effect on cell proliferation and invasion. Methods The surgically resected specimens of 47 GBC patients were collected in Lihuili Hospital Affiliated to Ningbo University from January 2017 to December 2020. There were 26 females and 21 males, with the age (62.0±8.2) years. The expression of CXCL11 protein in GBC tissues and corresponding paracancer tissues was detected by immunohistochemistry. Associations between CXCL11 expression and clinicopathological features were analyzed. After co-culturing of GBC-SD cells with exogenous CXCL11, cell counting kit-8 (CCK-8) and Transwell assays were performed to detect cell proliferation and invasion ability. The expression and phosphorylation level of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (Akt) were also detected by Western blot. Results The positive expression rate of CXCL11 in GBC tissues was significantly higher than that in adjacent paracancerous tissues [63.8% (30/47) vs 31.9% (15/47), χ2=9.59, P=0.002]. Furthermore, CXCL11 expression was significantly associated with tumor stage (χ2=6.64, P=0.010) and lymph nodal metastasis (χ2=7.86, P=0.005). CCK-8 assay revealed that the proliferation ability of GBC-SD cells in CXCL11-treated group significantly increased than that in the control group (absorbance value: 0.59±0.06 vs 0.32±0.04, t=9.64, P<0.001). Transwell assay showed that the cell invasion ability in CXCL11-treated group significantly increased than that in the control group [number of transmembrane cells: (133.4±12.3) cells vs (38.6±4.4) cells, t=16.21, P<0.001]. Western blot analysis showed that the relative expression levels of phosphorylated PI3K (p-PI3K) and phosphorylated Akt (p-Akt) in CXCL11-treated group (0.88±0.06 and 0.83±0.04) were significantly higher than those in the control group (0.17±0.04 and 0.23±0.06), and the differences were statistically significant (t=18.54, P<0.001 and t=15.21, P<0.001). Conclusion CXCL11 is highly expressed in GBC and closely related to tumor progression. CXCL11 can promote the proliferation and invasion of GBC cells via PI3K/Akt signaling pathway.
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