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CXCR 4 enhances cisplatin resistance of human tongue squamous cell carcinoma
Author(s) -
Zhuang XiuMei,
Zhou Bin
Publication year - 2019
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12813
Subject(s) - cisplatin , apoptosis , transfection , cancer research , cell growth , flow cytometry , cyclin d1 , biology , small interfering rna , microbiology and biotechnology , cell cycle , cell culture , medicine , chemotherapy , biochemistry , genetics
Background The chemokine receptor 4 ( CXCR 4) plays an important role in tumor progression. Overexpressed CXCR 4 is associated with a poor prognosis of patient with head and neck squamous cell carcinomas. However, the correlation between CXCR 4 and chemotherapy resistance in tongue squamous cell carcinoma ( TSCC ) remains obscure. Methods Stable cisplatin‐resistant CAL 27 CDDP and SCC 25 CDDP cells were established and identified by CCK 8 assay, and the CXCR 4 expression was detected using qRT ‐ PCR and Western blot. CXCR 4‐si RNA was transfected into TSCC CDDP cells, whose transfect efficiency was examined. Cisplatin sensitivity was further detected, as well as several proliferation and apoptosis‐related proteins. Results CAL 27 CDDP and SCC 25 CDDP cells were successfully established, which exhibited significantly higher cell viability and less apoptosis under cisplatin stimulation than that of parental cells. CXCR 4 expression was increased in TSCC CDDP cells. After transfection of CXCR 4‐si RNA , the expression of CXCR 4 was reduced by 73% and 78% in CAL 27 CDDP and SCC 25 CDDP cells, respectively. CCK 8 assay and flow cytometry assay revealed that the proliferative capacity under cisplatin stimulation significantly decreased after CXCR 4 silencing. Moreover, increased TSCC CDDP cells were arrested in the G0/G1 phase after knockdown of CXCR 4. Compared with negative control group, the expression of cyclin D1 and p‐ AKT decreased, while that of p‐caspase‐3 and Bax significantly increased. Conclusions Silencing CXCR 4 may evidently inhibit proliferation, induce apoptosis and enhance cisplatin sensitivity of TSCC CDDP cells by reduced cyclin D1 and p‐ AKT , and increased p‐caspase‐3 and Bax.