MEX3A (Mex-3 RNA Binding Family Member A)

MEX3A contributes to colorectal carcinogenesis, in association with PPARγ signalling modulation, impacting tumor development and therapeutic response.

Silencing PCBP2 in CCA cells did not alter the response to anti-CCA drugs (cisplatin, oxaliplatin, gemcitabine, 5-fluorouracil, and sorafenib) but reduced cell viability and proliferation, impaired colony formation, and inhibited migration. Electrophoretic mobility shift assay (EMSA) demonstrated that PCBP2 binds to the DHRS3 3'UTR, suggesting a role for PCBP2 in the post-transcriptional regulation of its target genes. In conclusion, PCBP2 promotes the malignant phenotype in CCA, highlighting its potential as a target for the development of future pharmacological treatments for patients with this cancer.

Among them, MEX3D emerges as a particularly promising prognostic biomarker. These findings establish a foundation for future mechanistic and translational studies exploring MEX3 family members as potential biomarkers or therapeutic targets in glioma.

MEX3A overexpression recused the tumor-inhibitory regulation of matrine in CRC cells. Matrine also repressed tumor growth of CRC in vivo through downregulating MEX3A. This study revealed that matrine played a cancer-suppressive role in CRC through targeting METTL14/MEX3A network, unraveling a molecular mechanism of matrine in CRC inhibition.

In summary, MEX3A promotes the aggressiveness of breast cancer via regulating the seRNA m6A/RBM15B/IGF2BP3/KMT2C axis. Therefore, targeting the MEX3A/seRNA m6A/RBM15B-IGF2BP3/KMT2C axis may be a therapeutic target for breast cancer.

With regard to MEX3A and cancer stem cells, it is necessary to assess the effect of MEX3A on cancer stem cell self-renewal and use organoids to test the targeting ability of MEX3A-inhibitors. In addition, improvements such as larger-scale validation and in-depth mechanism research are required, which could boost hepatocellular carcinoma understanding and patient prognosis.

A recent study by Ji et al highlights MEX3A's role in driving proliferation and migration via the RORA/β-catenin axis and epithelial-mesenchymal transition, positioning it as a potential biomarker and therapeutic target. This study addresses a critical gap in understanding HCC pathogenesis and offers valuable mechanistic insights.

Notably, MEX3A knockdown inhibits tumor growth in vitro and in vivo. Our findings highlight MEX3A as a novel diagnostic and prognostic biomarker and a promising therapeutic target for GB.

The present review aimed to summarize the molecular functions, tumor‑specific roles and translational relevance of MEX3A, bridging the gap between mechanistic insight and clinical applications. Future studies exploring MEX3A‑targeted interventions may reveal novel strategies for precision oncology.

To synthesize our results, this study identified that MEX3A in LUAD promoted malignancy of the disease by enhancing JAK-STAT signaling, which in turn inhibited cytotoxic capabilities of NK cells, thus providing novel insights for LUAD immunotherapy.

Our findings suggest that the MEX3 family is associated with the prognosis of hepatocellular carcinoma patients and contributes to disease progression by modulating the cell cycle and protein post-transcriptional modifications. Furthermore, this family is related to the tumor microenvironment, particularly in hypoxia and immune responses, which holds significant value for predicting liver cancer outcomes.

Further, we highlighted how these prognostic markers correlated to clinical parameters such as tumor node metastasis, tumor diameter, differentiation, hepatocirrhosis, vascular invasion, and others in HCC. Therefore, identifying specific prognostic biomarkers of HCC helps to provide a great opportunity to improve the prognosis in patients with HCC and provide therapeutic targets.