FAM72A (Family With Sequence Similarity 72 Member A)

We further developed a robust FAM72 gene signature to predict the prognosis of patients with liver cancer, and the gene signature was associated with immune infiltration. Collectively, these findings indicate the involvement of the FAM72 family in liver tumorigenesis and suggest its potential utility as a biomarker for adverse prognostic outcomes.

Epirubicin exerts anti-myeloma effects by downregulating CDC20 and inducing cell-cycle arrest in MM, highlighting CDC20 as a potential biomarker for identifying MM patients likely to benefit from epirubicin.

The role of FAM72A in the PI3K/AKT/mTOR pathway was further evaluated by Western blot and pharmacological modulation with the activator 740 Y-P and the inhibitor LY294002...Conversely, FAM72A overexpression enhanced these malignant traits. In vivo, FAM72A knockdown reduced tumor burden and altered EMT markers and PI3K/AKT/mTOR pathway activity. FAM72A promotes CC progression, at least in part, through activation of the PI3K/AKT/mTOR pathway, supporting its value as a potential therapeutic target.

FAM72A inhibits cellular pyroptosis by decreasing ROS levels, which in turn promotes the proliferation and invasion of CRC cells, and it is expected to be a potential therapeutic target for CRC.

However, only FAM72A is able to bind to and induce UNG2 degradation in human cells. Our results suggest that the ability of FAM72A to induce UNG2 degradation contributes to neoplasia in a variety of cancer types by promoting mutagenic repair of genomic dUs.

These findings indicate that the FAM72 gene family is a potential molecular marker for poor prognosis in LIHC, providing additional insights into the development of therapeutic approaches and prognostic markers.

While FAM72's presence as a gene pair with the SLIT-ROBO Rho GTPase-activating protein 2 (SRGAP2) is intriguing, its functional roles, particularly in neural stem cells, remain incompletely understood. This review explores the distinct characteristics of FAM72, shedding light on its expression patterns, potential roles in cell cycle regulation, stem cell renewal and implications in neurogenesis and tumorigenesis.

Our study further suggests that FAM72A hijacks the CTLH complex to promote mutagenesis in cancer. These findings show that FAM72A is an E3 ligase substrate adaptor critical for humoral immunity and cancer development.

Overexpression of FAM72A promotes U266 cell proliferation, inhibits apoptosis, and reduces sensitivity to bortezomib by regulating the POU2F2/FAM72A/p53 signaling pathway.

This study successfully developed and validated novel biomarkers based on FFGs for predicting the prognosis and immune status of UCEC patients. The identified FFGs can accurately assess the prognosis of UCEC patients and facilitate the identification of specific subgroups of patients who may benefit from personalized treatment with immunotherapy and chemotherapy.

Our findings indicate that FAM72B and FAM72C are potential molecular markers of poor prognosis in OSCC and may act as novel targets for OSCC treatment strategies.

All of these data indicate that FAM72A confers an aggressive phenotype and poor prognosis on gliomas. Targeting FAM72A might represent a new therapeutic strategy for glioma.