Tns4, also known as Tensin4 or Cten, is a putative oncogene. It plays roles in regulating cell adhesion, motility, invasion, and epithelial to mesenchymal transition (EMT) [3]. Tns4 is involved in multiple signaling pathways such as Wnt, JAK2-STAT3, and EGFR signaling, which are crucial in various biological processes and disease development [1,2,4].

In ApcMin/+ mice, an animal model of colorectal cancer, Tns4 was upregulated in intestinal adenomas by Wnt signalling, suggesting its potential role in adenoma development [2]. In colorectal cancer cell lines, Tns4 knockdown increased cell proliferation in compact-spheroid-producing lines, reduced adhesiveness and 3D invasion, and enhanced sensitivity to the EGFR inhibitor gefitinib [3]. In gallbladder cancer, knocking down GPRC5A led to down-regulation of Tns4 through the JAK2-STAT3 axis, and GPRC5A-mediated up-regulation of Tns4 promoted cancer cell metastasis [1].

In conclusion, Tns4 is significantly associated with cancer-related biological processes. Findings from gene-knockdown experiments in mouse models and cell lines demonstrate its role in cancer progression, especially in colorectal and gallbladder cancers. Understanding Tns4's function provides potential therapeutic targets for these diseases.