Tspan13, short for Tetraspanin 13, is a cell-surface protein. Tetraspanins are known to play critical roles in many cellular processes. Although not explicitly stated in the references about its core function, its involvement in signaling pathways is evident. For example, it activates the CXCR4/CXCL12 signaling pathway [1].

In leukemia, Tet2 deficiency leads to an increase in Tspan13 expression. This increase promotes the homing of leukemia stem cells (LSCs) into the bone marrow niche, enhancing their self-renewal and proliferation. Mechanistically, Tet2 deficiency causes m5C modification accumulation in Tspan13 mRNA, which is recognized by YBX1, increasing Tspan13 transcript stability and expression [1].

In papillary thyroid cancer (PTC), the down-regulation of miR-369-3p leads to up-regulation of Tspan13, promoting cell proliferation [2].

In breast cancer, miR-4732-5p targets the 3'-UTR of Tspan13, suppressing its expression. miR-4732-5p may act as a tumor suppressor in breast cancer initiation but a promoter in progression [3].

In osteosarcoma, hTERT promotes tumor progression by enhancing Tspan13 expression, and knocking down Tspan13 in hTERT-overexpressing cells enhances apoptosis and suppresses mesenchymal properties [4].

In prostate cancer, Tspan13 is overexpressed, and its expression inversely correlates with Gleason score and PSA preoperative levels, while directly correlating with the presence of prostatic intraepithelial neoplasia [5].

In conclusion, Tspan13 is involved in multiple disease-related cellular processes. Its dysregulation is associated with leukemia, thyroid cancer, breast cancer, osteosarcoma, and prostate cancer. Through functional studies, mainly in in-vivo-like scenarios where gene expression is manipulated, we can see its role in cell proliferation, migration, and homing, providing insights into the disease mechanisms and potential therapeutic targets.