Liu Ruoyan, Shuai Yanjie, Luo Jingtao, Zhang Ze
Department of Gynecologic Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Front Oncol. 2019 Oct 9;9:1035. doi: 10.3389/fonc.2019.01035. eCollection 2019.
Aberrant activation of Semaphorin3C(SEMA3C) is widespread in human cancers. We aimed to analyze SEMA3C expression in cervical cancer and investigate the role of SEMA3C in cervical cancer and its underlying mechanism, which is important for exploring new therapeutic targets and prognostic factors. The expression of SEMA3C was examined in paraffin-embedded cervical cancer specimens. and assays were performed to validate the effect of SEMA3C on cervical cancer cell proliferation and p-ERK pathway activation. Gene Set Enrichment Analysis (GSEA) was performed using The Cancer Genome Atlas (TCGA) data set. SEMA3C expression was associated with poor survival in both the TCGA cohort and our cohort. Silencing of SEMA3C suppressed cervical cancer cell proliferation, colony formation ability, and the activation of the p-ERK signaling pathway . SEMA3C depletion inhibited tumor growth . GSEA also showed that the epithelial mesenchymal transition (EMT), TGFβ signaling pathway, angiogenesis, and extracellular matrix (ECM) receptor interactions are associated with a high SEMA3C expression phenotype. SEMA3C is correlated with poor prognosis of cervical cancer patients and promotes tumor growth via the activation of the p-ERK pathway.
信号素3C(SEMA3C)的异常激活在人类癌症中广泛存在。我们旨在分析SEMA3C在宫颈癌中的表达情况,并研究SEMA3C在宫颈癌中的作用及其潜在机制,这对于探索新的治疗靶点和预后因素具有重要意义。在石蜡包埋的宫颈癌标本中检测SEMA3C的表达。并进行实验以验证SEMA3C对宫颈癌细胞增殖和p-ERK通路激活的影响。使用癌症基因组图谱(TCGA)数据集进行基因集富集分析(GSEA)。在TCGA队列和我们的队列中,SEMA3C表达均与较差的生存率相关。沉默SEMA3C可抑制宫颈癌细胞增殖、集落形成能力以及p-ERK信号通路的激活。SEMA3C缺失抑制肿瘤生长。GSEA还表明,上皮-间质转化(EMT)、TGFβ信号通路、血管生成和细胞外基质(ECM)受体相互作用与高SEMA3C表达表型相关。SEMA3C与宫颈癌患者的不良预后相关,并通过激活p-ERK通路促进肿瘤生长。