Tm2d1-KO Mouse

Tm2d1, also known as β -amyloid peptide binding protein, is critical to the pathogenesis of Alzheimer's disease (AD). It may be involved in the intracellular signaling pathways related to β -amyloid peptide-induced neuronal cell death, though it doesn't directly couple to Gα(i/o), Gα(s), or Gα(q) proteins [3,4].

In hepatocellular carcinoma (HCC), TM2D1 is increasingly expressed in tumors compared to peritumoral tissues. Overexpression of TM2D1 promotes HCC cell proliferation, migration, and invasion, related to epithelial-mesenchymal transition (EMT) by activating the AKT/β-catenin axis. Depletion of TM2D1 leads to the opposite phenotype [1]. In colorectal cancer, sevoflurane and propofol co-treatment affects cancer cell biology behaviors such as apoptosis, ferroptosis, proliferation, invasion, and migration, with TM2D1 considered a target. Overexpression of TM2D1 reverses these effects [2].

In conclusion, Tm2d1 plays important roles in the development of certain cancers. In HCC, it promotes EMT through the AKT/β-catenin axis, and in colorectal cancer, it is involved in the anti-tumor mechanism of sevoflurane and propofol. These findings suggest Tm2d1 could be a potential therapeutic target for these cancers.

References:

1. Hu, Jin-Wu, Yin, Yue, Gao, Yang, Fan, Jia, Zhou, Jian. 2021. TM2D1 contributes the epithelial-mesenchymal transition of hepatocellular carcinoma via modulating AKT/β-catenin axis. In American journal of cancer research, 11, 1557-1571. doi:. https://pubmed.ncbi.nlm.nih.gov/33948373/

2. Lu, Yan, Li, Ling, Piao, Zongfang, Tan, Xinmin, Su, Rui. 2024. Sevoflurane and Propofol Co-affect the Development of Colorectal Cancer by Regulating TM2D1. In Combinatorial chemistry & high throughput screening, , . doi:10.2174/0113862073281046240527165415. https://pubmed.ncbi.nlm.nih.gov/38920064/

3. Lee, Yong, Chang, Deok-Jin, Lee, Yong-Seok, Suh, Yoo-Hun, Kaang, Bong-Kiun. . Beta-amyloid peptide binding protein does not couple to G protein in a heterologous Xenopus expression system. In Journal of neuroscience research, 73, 255-9. doi:. https://pubmed.ncbi.nlm.nih.gov/12836168/

4. Kajkowski, E M, Lo, C F, Ning, X, Jacobsen, J S, Ozenberger, B A. 2001. beta -Amyloid peptide-induced apoptosis regulated by a novel protein containing a g protein activation module. In The Journal of biological chemistry, 276, 18748-56. doi:. https://pubmed.ncbi.nlm.nih.gov/11278849/