FAM107A, Family with sequence similarity 107 member A, has been recognized as a potential tumor suppressor in various malignancies. It is involved in regulating tumor cell proliferation, migration, invasion, and apoptosis. In terms of associated pathways, it has been linked to the FAK/PI3K/AKT signaling pathway [2], and KEGG and GO enrichment analysis suggest "cell adhesion" and "cAMP signaling pathway" as potential impacts [4]. Genetic models are valuable for further exploring its functions.

In multiple cancers, including esophageal squamous carcinoma [1], prostate cancer [2], bladder cancer [3], lung adenocarcinoma [5], non-small cell lung cancer [6], and colorectal cancer [7], FAM107A shows reduced expression. In these cases, low FAM107A expression is associated with poor prognosis and unfavorable clinicopathological characteristics. Overexpression of FAM107A in cancer cell lines and in vivo xenograft models inhibits tumor cell growth, invasion, migration, and the epithelial-mesenchymal transition process, and promotes apoptosis. For example, in prostate cancer, its inactivation due to promoter methylation affects cancer progression through the FAK/PI3K/AKT pathway [2]. In bladder cancer, restoring FAM107A suppresses cell growth, migration, and invasion [3].

In summary, FAM107A functions as a potential tumor suppressor, inhibiting the malignant behavior of cancer cells. Studies using cell lines and in vivo models, such as xenograft tumors, have revealed its significance in cancer development. Understanding FAM107A's role provides potential therapeutic targets for cancers like esophageal squamous carcinoma, prostate cancer, bladder cancer, and others.