Journal of Medical Molecular Biology ›› 2022, Vol. 19 ›› Issue (6): 457-463.doi: 10.3870/j.issn.1672-8009.2022.06.004

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Effect of CD168 on Proliferation and Invasion of Oral Squamous Cell Carcinoma and Its Mechanism

  

  1. 1 Department of Stomatology, Fourth Hospital of Hebei Medical University, Shijiazhuang, 050011, China  2 Department of Stomatology, Children’s Hospital of Hebei Province, Shijiazhuang, 050031, China
  • Online:2022-11-30 Published:2023-02-14
  • Supported by:
    Key Science and Technology Research Plan of Hebei Provincial Health Commission (No. 20180526)

Abstract: Objective To explore the effect of CD168 on the proliferation and invasion of oral squamous cell carcinoma and its underlying mechanism. Methods The expression level of CD168 in the human normal oral keratinocyte cell line HOK and several oral squamous cell carcinoma cell lines was compared, and HN13 cell line was selected for the follow-up researches. Gene and protein expression levels of CD168 in cells infected with CD168 shRNA lentivirus were detected by using RT-qPCR and Western blotting. CCK-8 method was applied for the assay of the cell proliferation, the flow cytometry was used for the assay of cell apoptosis and the transwell assay was adopted to detect the cell invasion. Western blotting was performed to detect the expression levels of proteins related to cell proliferation, apoptosis, invasion and CXCL12-CXCR4 / CXCR7 signaling axis. Results The HN13 control cell line and the CD168-shRNA2 cell line were used for further studies (P < 0. 05). Silencing CD168 could suppress the proliferation and invasion of HN13 cells and increase its apoptosis rate (P< 0. 05). The protein expression levels of VEGF, PCNA, MMP-2, MMP-9, CXCL12, CXCR4 and CXCR7 were decreased in the shCH168 cells (P< 0. 05), while the Bax / Bcl-2 ratio was increased ( P < 0. 05), with no statistical changes observed between the shRNA-NC group and the control group (P > 0. 05). Conclusion Silencing of CD168 can inhibit the proliferation and invasion of oral squamous cell carcinoma cell line HN13, and promote their apoptosis, the mechanism may be related to the CXCL12-CXCR4 / CXCR7 signaling axis. 

Key words: oral squamous cell carcinoma, CD168, short hairpin RNA, cell proliferation; cell invasion, CXCL12-CXCR4 / CXCR7 signaling axis

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