Tes, also known as testin LIM domain protein, is a candidate tumor suppressor gene [1]. It contains three LIM domains, which are regions for interacting with cell adhesion and cytoskeleton regulatory proteins. TES may play a role in the regulation of cell adhesion, motility, and proliferation through its interactions with relevant proteins, and thus has biological importance in tumor-related processes [1].

In gastric cancer, TES has been shown to suppress cell proliferation, colony formation, induce cell cycle arrest, and inhibit tumorigenicity in vitro, as well as inhibit cell migration, invasion in vitro and metastasis in vivo [1]. It interacts with Mena, a cytoskeleton regulator, and inhibits the interaction of Mena with Lamellipodin (Lpd), functioning as a Mena-dependent tumor suppressor [1]. In GC patients with high Mena expression, the expression of TES is associated with tumor infiltration, lymph node metastasis, TNM stage, and prognosis [1].

In conclusion, Tes functions as a tumor suppressor in gastric cancer, especially in a Mena-dependent manner. The study of Tes in gastric cancer through in-vivo and functional studies helps to understand the mechanisms of gastric cancer carcinogenesis and metastasis, providing potential prognostic markers and treatment targets for gastric cancer [1].

References:

1. Wang, Dan-Dan, Chen, Yi-Bing, Zhao, Jing-Jing, Wang, Lei-Lei, Xia, Jian-Chuan. 2019. TES functions as a Mena-dependent tumor suppressor in gastric cancer carcinogenesis and metastasis. In Cancer communications (London, England), 39, 3. doi:10.1186/s40880-019-0347-y. https://pubmed.ncbi.nlm.nih.gov/30728082/