Fam53b, also known as Simplet, is a vertebrate-specific gene belonging to a family with no characterized biochemical domains. It is essential for cell proliferation and is involved in the Wnt/β-catenin signaling pathway, regulating β-catenin nuclear localization, which is crucial for many biological phenomena like cell fate determination and stem cell maintenance [3,5].

In pancreatic ductal adenocarcinoma (PDAC), FAM53B promotes metastasis by regulating macrophage M2 polarization. Blocking FAM53B in a murine model prevented tumor cell invasion and metastasis, suggesting its key role in PDAC pathogenesis [2].

In papillary thyroid carcinoma (PTC), circ_FAM53B (a circular RNA derived from the FAM53B gene) was found to be reduced. Overexpression of circ_FAM53B restrained PTC cell proliferation, migration, invasion, and triggered apoptosis, as well as hindered HUVEC tube formation. It exerted these effects via the miR-183-5p-CCDC6 axis [1].

In ovarian cancer, circ-FAM53B was overexpressed and accelerated cell proliferation, migration, and invasion. It functioned as a competing endogenous RNA, sponging miR-646 and miR-647 to upregulate VAMP2 and MDM2 expression [4].

In summary, Fam53b and its associated circular RNAs play significant roles in regulating cell proliferation and are involved in the pathogenesis of multiple cancers, including PDAC, PTC, and ovarian cancer. Research on Fam53b, especially through in vivo models like murine models, has provided insights into its functions and potential as a therapeutic target in these disease areas.