Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan.
Department of Pathology, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan.
Sci Rep. 2019 Nov 5;9(1):16055. doi: 10.1038/s41598-019-52227-0.
Transient receptor potential vanilloid 2 (TRPV2) was recently shown to be involved in migrant potentials. The present study aimed to investigate its role in esophageal squamous cell carcinoma (ESCC).
Knockdown experiments were conducted using TRPV2 siRNA in human ESCC cell lines, and anti-tumor effects were analyzed. The gene expression profiles of cells were analyzed using a microarray method. An immunohistochemical staining was performed on 62 primary tumor samples.
TRPV2 overexpression was observed in TE15 and KYSE170 cells. TRPV2 depletion suppressed proliferation, cell cycle progression, and invasion/migration ability, and induced apoptosis. A pathway analysis of microarray data showed that TRPV2 depletion down-regulated WNT/β-catenin signaling-related genes and basal cell carcinoma signaling-related genes. The suppression of tumor functions, such as proliferation, invasion, and angiogenesis, was predicted in the ontology analysis. Immunohistochemical analysis revealed a correlation between strong TRPV2 expression and a poor prognosis in ESCC patients.
The present results suggest that TRPV2 regulates cancer progression by affecting WNT/β-catenin or basal cell carcinoma signaling, and that TRPV2 strong expression is associated with a worse prognosis in ESCC patients. These results provide an insight into the role of TRPV2 as a novel therapeutic target or biomarker for ESCC.
瞬时受体电位香草酸 2(TRPV2)最近被证明参与了游走电位。本研究旨在探讨其在食管鳞状细胞癌(ESCC)中的作用。
使用 TRPV2 siRNA 在人 ESCC 细胞系中进行敲低实验,并分析抗肿瘤作用。使用微阵列方法分析细胞的基因表达谱。对 62 个原发性肿瘤样本进行免疫组织化学染色。
在 TE15 和 KYSE170 细胞中观察到 TRPV2 过表达。TRPV2 耗竭抑制增殖、细胞周期进程和侵袭/迁移能力,并诱导细胞凋亡。微阵列数据分析的通路分析表明,TRPV2 耗竭下调了 WNT/β-catenin 信号相关基因和基底细胞癌信号相关基因。本体论分析预测 TRPV2 抑制肿瘤功能,如增殖、侵袭和血管生成。免疫组织化学分析显示,TRPV2 强表达与 ESCC 患者预后不良相关。
本研究结果表明,TRPV2 通过影响 WNT/β-catenin 或基底细胞癌信号来调节癌症进展,并且 TRPV2 强表达与 ESCC 患者预后不良相关。这些结果为 TRPV2 作为 ESCC 的新型治疗靶点或生物标志物提供了新的见解。