Transgelin overexpression in lung adenocarcinoma is associated with tumor progression

肺腺癌中 Transgelin 的过表达与肿瘤进展有关

阅读:9
作者:Xiaohong Wu, Liangliang Dong, Ruifeng Zhang, Kejing Ying, Huahao Shen

Abstract

Hypoxia is a common feature of solid tumors and is associated with an increased likelihood of local recurrence and distant metastasis. Transgelin (TAGLN) is an actin cross-linking/polymerization protein that belongs to the family of actin-associated proteins, and there is evidence that TAGLN may be involved in the migration of epithelial cells by interacting with actin or promoting podosome formation. Cell migration is a key step of cancer metastatis. Thus, the aim of this study was to investigate the potential link between TAGLN protein levels and hypoxia in lung adenocarcinoma cells and to explore the possible functions and expression patterns of TAGLN in lung adenocarcinoma. We first examined the effects of altered TAGLN expression on cell migration under both normoxic and hypoxic conditions. Immunohistochemical (IHC) staining was also performed to examine TAGLN protein expression patterns in lung adenocarcinoma samples. Our results revealed that TAGLN was upregulated in the hypoxic lung adenocarcinoma cells. The inhibition of TAGLN expression in the cells using small interfering RNA (siRNA) led to a decreased migration ability. TAGLN was significantly overexpressed in the lung adenocarcinoma tissues compared to the adjacent tumor-free tissues. A high TAGLN expression correlated with an advanced TNM stage, lymph node metastasis and greater differentiation. TAGLN was upregulated in the human lung adenocarcinoma cell lines under hypoxic conditions, which contributed to the migration ability of the cells. Thus, our data suggest that TAGLN may be a viable therapeutic target and a potential biomarker for predicting the prognosis of patients with lung adenocarcinoma.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。