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FAM84A was identified through genome-wide cDNA microarray analysis, which revealed its frequent upregulation in colorectal cancer tissues . This gene was not expressed in any of the 23 normal tissues examined, except for the testis . The gene was cloned by researchers who noted its 44% amino acid identity with FAM84B and 34.5% identity with the C. elegans cuticle collagen-12 precursor .
The expression of FAM84A mRNA and protein has been confirmed to be upregulated in colorectal carcinomas compared to normal colonic mucosa . Additionally, FAM84A expression has been observed in bladder, pancreatic, and lung cancers . Immunocytochemical studies have localized FAM84A to the subplasma membrane region, particularly in areas where cells do not have contact with neighboring cells .
FAM84A plays a crucial role in cell migration and morphology. Studies have shown that exogenous expression of FAM84A increases cell motility in NIH3T3 cells . The phosphorylation of serine 38 of FAM84A is associated with changes in cell morphology, suggesting that this post-translational modification is important for its function . Wound healing and transwell assays have demonstrated that FAM84A significantly enhances cell migration and wound filling .
The upregulation of FAM84A in colorectal cancer and its role in enhancing cell motility suggest that it may play a critical role in cancer progression . Understanding the molecular mechanisms by which FAM84A contributes to cancer cell migration and invasion could provide insights into potential therapeutic targets for colorectal and other cancers.