口腔医学研究 ›› 2023, Vol. 39 ›› Issue (12): 1085-1091.DOI: 10.13701/j.cnki.kqyxyj.2023.12.011

• 口腔肿瘤学研究 • 上一篇    下一篇

SDC4在唾液腺腺样囊性癌神经侵袭中的作用研究

张艳宁1, 石宏2*, 李荷香3, 王洁3, 郝亚丽1, 王旭4, 袁云云1   

  1. 1.河北医科大学口腔医学院·口腔医院,河北省口腔医学重点实验室,河北省口腔疾病临床医学研究中心 河北 石家庄 050017;
    2.河北医科大学口腔医学院·口腔医院儿童口腔科 河北 石家庄 050017;
    3.河北医科大学口腔医学院·口腔医院病理科 河北 石家庄 050017;
    4.河北医科大学口腔医学院·口腔医院修复科 河北 石家庄 050017
  • 收稿日期:2023-06-08 出版日期:2023-12-28 发布日期:2023-12-25
  • 通讯作者: * 石宏,E-mail:shihong_hb@163.com
  • 作者简介:张艳宁(1984~ ),女,河北人,博士,副教授,研究方向:口腔颌面部肿瘤。
  • 基金资助:
    河北省自然科学基金(编号:H2017206234)河北省科技厅卫生健康创新专项(编号:22377755D)河北省政府资助省级医学优秀人才项目(编号:361029)

Role of SDC4 in Perineural Invasion of Salivary Adenoid Cystic Carcinoma

ZHANG Yanning1, SHI Hong2*, LI Hexiang3, WANG Jie3, HAO Yali1, WANG Xu4, YUAN Yunyun1   

  1. 1. Hebei Key Laboratory of Stomatology, Hebei Clinical Research Center for Oral Diseases, School and Hospital of Stomatology, Hebei Medical University, Shijiazhuang 050017, China;
    2. Department of Pediatric Dentistry, School and Hospital of Stomatology, Hebei Medical University, Shijiazhuang 050017, China;
    3. Department of Oral Pathology, School and Hospital of Stomatology, Hebei Medical University, Shijiazhuang 050017, China;
    4. Department of Prosthodontics, School and Hospital of Stomatology, Hebei Medical University, Shijiazhuang 050017, China
  • Received:2023-06-08 Online:2023-12-28 Published:2023-12-25

摘要: 目的:探讨SDC4在CXCL12介导的唾液腺腺样囊性癌周围神经侵袭中的作用。方法:Transwell趋化试验检测不同浓度CXCL12对SACC-83细胞的趋化性;细胞免疫荧光染色和免疫共沉淀分析SDC4与CXCL12的相互作用;构建靶向敲低SDC4基因的shRNA慢病毒表达载体,敲低SDC4在SACC-83细胞的表达;CCK-8法、细胞划痕和Transwell趋化试验检测细胞增殖、迁移和趋化性;采用裸鼠体内周围神经侵袭模型检测周围神经侵袭能力。结果:CXCL12促进SACC-83细胞迁移,并与其浓度呈正相关(P<0.01); SDC4与CXCL12有相互作用,SDC4基因敲低后,SACC-83细胞在CXCL12诱导下的迁移和趋化性均明显降低(P<0.05),而细胞增殖能力没有明显改变(P>0.05),同时裸鼠体内试验表明,其周围神经侵袭能力明显降低(P<0.05)。结论:SDC4通过与CXCL12相互作用参与腺样囊性癌的周围神经侵袭过程。

关键词: 腺样囊性癌, SDC4, CXCL12, 周围神经侵袭

Abstract: Objective: To investigate the role of SDC4 in the perineural invasion of salivary adenoid cystic carcinoma induced by CXCL12. Methods: Transwell assay was used to evaluate the influence of different concentrations of CXCL12 on the chemotaxis of SACC-83 cells. Immunofluorescence staining and co-immunoprecipitation were performed to validate the interactions between SDC4 and CXCL12. The expression of SDC4 in the SACC-83 cells was silenced by viral transfection by constructing lentivirus-expressing shRNA targeting SDC4. The effect of SDC4 silencing on the proliferation and migration was assessed via the CCK-8, wound healing, and transwell assays. An in vivo perineural invasion model was used to prove the effect of SDC4 silencing on the perineural invasion of the SACC-83 cells. Results: CXCL12 induced the migration of SACC-83 cell in a concentration-dependent manner (P<0.01). Co-immunoprecipitation studies validated these interactions between SDC4 and CXCL12. Furthermore, SDC4 gene expression was silenced by RNAi and verified by real-time polymerase chain reaction and western blotting analysis. The migration and chemotactic efficiency of the SACC-83 cells induced by CXCL12 were significantly decreased via SDC4 silencing (P<0.05). While the proliferation of the SACC-83-SDC4-silenced cells showed no difference compared to that of SACC-83 cells (P>0.05). The perineural invasion ability was significantly inhibited by SDC4 silencing in vivo (P<0.05). Conclusion: SDC4 involved in the perineural invasion of salivary adenoid cystic carcinoma through interaction with CXCL12.

Key words: salivary adenoid cystic carcinoma, SDC4, CXCL12, perineural invasion