Ctf1-flox Mouse

Ctf1, also known as cardiotrophin 1, is involved in multiple biological processes. It activates autophagy in fibroblasts and carcinoma-associated fibroblasts (CAFs) through stimulating phosphorylation and nuclear translocation of STAT3, and is associated with pathways like AMPK and ULK1 activation. It plays a key role in tumor-stroma interactions, fibroblast activation, and cancer metastasis [1]. In the context of glioma, it may be related to tumor progression pathways such as IL2_STAT5, P53, and IL6_JAK_STAT3 signaling pathways, and is associated with immune cell infiltration [2].

In breast cancer, tumor-derived Ctf1 promotes breast cancer cell migration, invasion, and metastasis in an autophagy-dependent manner [1]. In glioma, its high expression is associated with poorer survival, advanced grades, and is an independent risk factor. Also, in glioma, it shows associations with drug sensitivity and immune infiltration [2,5]. Exosomes from Ctf1-modified bone marrow stem cells can promote endometrial regeneration and restore fertility, likely through upregulating the JAK/PI3K/mTOR/STAT3 signaling pathways [3]. In the skin, Ctf1-IL6ST signaling from dermal papilla to endothelial cells promotes angiogenesis during aging [4].

In summary, Ctf1 is crucial in various biological processes and disease conditions. Its role in promoting cancer-related events like metastasis in breast cancer and its associations with prognosis and immune microenvironment in glioma are significant. Also, its potential in endometrial regeneration and angiogenesis in the skin showcases its diverse functions. The study of Ctf1 using various models helps in understanding disease mechanisms and potential therapeutic targets.