Tes, also known as testin LIM domain protein, is a candidate tumor suppressor gene. It contains three LIM domains which interact with cell adhesion and cytoskeleton regulatory proteins. TES may play a role in regulating cell adhesion, motility, and proliferation through its interactions with cytoskeleton-related proteins [1].

In gastric cancer, TES functions as a Mena-dependent tumor suppressor. In vitro cell proliferation assay, colony formation assay, cell cycle analysis, Transwell assays, and in vivo tumorigenicity and metastasis assays showed that TES suppressed gastric cancer cell proliferation, colony formation, induced cell cycle arrest, inhibited migration, invasion, and metastasis. TES interacted with Mena and inhibited the interaction of Mena with Lpd, suppressing cell migration and invasion in a Mena-dependent manner. In gastric cancer patients with high Mena expression, TES expression was associated with tumor infiltration, lymph node metastasis, TNM stage, and prognosis [1].

In conclusion, Tes is a tumor suppressor gene with potential significance in gastric cancer. Its function as a Mena-dependent tumor suppressor reveals its importance in regulating cancer-related biological processes such as carcinogenesis and metastasis. The study of Tes in gastric cancer using in vivo models provides insights into the mechanisms of cancer development and potential therapeutic targets [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/