河北医科大学学报 ›› 2023, Vol. 44 ›› Issue (5): 547-552.doi: 10.3969/j.issn.1007-3205.2023.05.010

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lncRNA SNHG12促进宫颈癌SiHa细胞迁移、侵袭和抑制细胞凋亡

  

  1. 河北医科大学第一医院妇产科,河北 石家庄 050031

  • 出版日期:2023-05-25 发布日期:2023-05-25
  • 作者简介:王旭（1987-)，女，河北石家庄人，河北医科大学第一医院主治医师，医学硕士，从事妇科肿瘤疾病诊治研究。
  • 基金资助:
    河北省医学科学研究课题计划（20211215）

lncRNA SNHG12 promotes mirgation, invasion and suppresses apoptosis of cervical cancer SiHa cells

  1. Department of Obstetrics and Gynecology, the First Hospital of Hebei Medical University, Shijiazhuang 050031, China

  • Online:2023-05-25 Published:2023-05-25

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摘要： 目的 探讨lncRNA核仁小分子宿主基因12(small nucleolar host gene12,SNHG12)对宫颈癌SiHa细胞增殖、周期、侵袭、迁移及凋亡的调控作用。
方法 采用实时荧光定量聚合酶链式反应（quantitative real-time polymerase chain reaction，qRT-PCR）检测SNHG12在宫颈癌组织和细胞株HaCaT，C33A，SiHa和CasKi中的表达；CCK8、流式细胞法、Transwell、细胞划痕及Tunel细胞凋亡法检测SNHG12对SiHa细胞增殖、周期、侵袭、迁移及凋亡的调控能力；检测宫颈癌皮下瘤体生长情况；免疫组织化学试验检测Ki67抗体。
结果 过表达SNHG12在宫颈癌组织和各细胞株中均显著升高；上调SNHG12能促进SiHa细胞增殖、周期、侵袭、迁移及抑制凋亡；SNHG12促进皮下瘤体生长，干扰SNHG12能产生抑制效果；SNHG12的阳性信号明显增加，而沉默SNHG12后结论相反。
结论 SNHG12可以促进宫颈癌SiHa细胞增殖、细胞周期、侵袭、迁移及抑制凋亡，进而参与宫颈癌的病理进程。


关键词: 宫颈肿瘤, 核仁小分子宿主基因12, 细胞增殖

Abstract: Objective To investigate the regulation of lncRNA small nucleolar host gene12 (SNHG12) on proliferation, cell cycle, invasion, migration and apoptosis of cervical cancer SiHa cells. 
Methods RT-PCR was performed to detect SNHG12 expression in cervical cancer tissues and cell lines HaCaT, C33A, SiHa and CasKi. CCK8, flow cytometry assay, Transwell, cell wound scratch assay and Tunel cell apoptosis were adopted to detect the regulatory abilities of SNHG12 on proliferation, cell cycle, invasion, migration and apoptosis of SiHa cells, and also to detect the subcutaneous tumor growth of cervical cancer. Immunohistochemistry was used to detect Ki67 antibodies. 
Results Overexpressed SNHG12 was obviously elevated in cervical cancer tissues and all cell lines. SNHG12 up-regulation could promote proliferation, cell cycle, invasion, migration and inhibit apoptosis of SiHa cells. SNHG12 could promote subcutaneous tumor growth, while interference with SNHG12 could generate inhibitory effects. The positive signal of SNHG12 was highly enhanced, while silencing SNHG12 produced the opposite result. 
Conclusion SNHG12 could facilitate SiHa cell proliferation, cell cycle, invasion, migration and suppress apoptosis, thereby participating in the pathological process of cervical cancer. 


Key words: cervical neoplasms, small nucleolar host gene12, cell proliferation

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