过度表达的 versican 促进胃癌细胞增殖、迁移和侵袭。

Overexpressed versican promoted cell multiplication, migration and invasion in gastric cancer.

机构信息

Department of Pathology, The First Hospital of Qiqihar, Affiliated Qiqihar Hospital, Southern Medical University, China.

出版信息

Tissue Cell. 2021 Dec;73:101611. doi: 10.1016/j.tice.2021.101611. Epub 2021 Aug 2.

DOI:10.1016/j.tice.2021.101611

PMID:34358918

Abstract

Versican (VCAN) is verified to promote development among many cancers, whose function on gastric cancer (GC) is less studied. This work explored the effect of VCNA on GC. The differentially expressed VCAN between tumor and normal samples, among different cancer stages and the overall survival of GC patients with high and low VCAN levels were predicted through Gene Expression Profiling Interactive Analysis 2 (GEPIA2). The association between VCAN and clinicopathological parameters was analyzed by clinical investigation. AGS and NCI-N87 cells were transfected with VCAN short hairpin RNA (shVCAN) and VCAN overexpression plasmid. The VCNA, Cyclin D1, Cyclin E, E-Cadherin, N-Cadherin and Vimentin expression was detected through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. Cell viability was assessed through MTT assay. Cell migration was measured by wound healing assay and cell invasion was evaluated through Transwell assay. Cell cycle was determined by flow cytometry assay. VCAN was upregulated in GC and its high expression related to advanced TNM stage, Lymph node metastasis, Depth of invasion and Grade. VCAN knockdown inhibited multiplication, migration, invasion, Cyclin D1, Cyclin E, N-Cadherin and Vimentin expression while induced cycle arrest and E-Cadherin level of GC cells, whereas overexpressed VCAN showed opposite results. VCAN had a potential to be a biomarker for GC and overexpressed VCAN promoted GC cell multiplication, migration and invasion.

摘要

神经钙黏蛋白（VCAN）已被证实可促进多种癌症的发展，但其在胃癌（GC）中的作用研究较少。本研究旨在探讨 VCNA 对 GC 的影响。通过基因表达谱交互分析 2（GEPIA2）预测肿瘤和正常样本、不同癌症阶段以及 VCNA 水平高和低的 GC 患者总生存率之间的差异表达 VCNA。通过临床研究分析 VCAN 与临床病理参数之间的关系。AGS 和 NCI-N87 细胞用 VCNA 短发夹 RNA（shVCAN）和 VCNA 过表达质粒转染。通过定量逆转录聚合酶链反应（qRT-PCR）和 Western blot 检测 VCNA、周期蛋白 D1、周期蛋白 E、E-钙黏蛋白、N-钙黏蛋白和波形蛋白的表达。通过 MTT 测定评估细胞活力。通过划痕愈合测定测量细胞迁移，通过 Transwell 测定评估细胞侵袭。通过流式细胞术测定确定细胞周期。GC 中 VCAN 上调，其高表达与较晚的 TNM 分期、淋巴结转移、浸润深度和分级有关。VCAN 敲低抑制 GC 细胞的增殖、迁移和侵袭，下调 Cyclin D1、Cyclin E、N-钙黏蛋白和波形蛋白的表达，同时诱导细胞周期停滞和上调 E-钙黏蛋白水平，而过表达 VCAN 则表现出相反的结果。VCAN 有可能成为 GC 的生物标志物，过表达的 VCAN 促进 GC 细胞增殖、迁移和侵袭。