VIRMA (Vir Like M6A Methyltransferase Associated)

Our study constructed a novel signature associated with m6A modifications, which can serve as a promising prognostic indicator for LUAD. These findings may provide valuable insights into diagnosis and therapeutic strategies for patients with LUAD.

In summary, m6A methyltransferase KIAA1429 suppressed CRC tumor immunity by upregulating PD-L1 expression and reducing CD8+T cells infiltration. Targeting KIAA1429 might improve CRC anti-tumor immunity and enhance the efficacy of CRC immunotherapy.

The outcomes of qRT-PCR, immunoblotting and MeRIP assay confirmed a positive association between KIAA1429 and FAM84B. Furthermore, KIAA1429 silencing partially decreased β-catenin levels and reversed the malignant effects of FAM84B overexpression on CRC cells, both in vitro and in vivo. The results illustrate that KIAA1429 promotes CRC tumorigenesis by stabilizing FAM84B mRNA and activating the Wnt/β-catenin pathway, highlighting its capability as a prognostic biomarker and therapeutic target for CRC.

Phosphorylated LDHA (Y10) promotes EV-circSEPT9 secretion, elevating intracellular circSEPT9 levels in recipient TNBC cells. By functioning as a competing endogenous RNA (ceRNA) that sponges miR-515-5p, circSEPT9 upregulates KIAA1429, augments m6A methylation, and drives the development of chemoresistance.

However, challenges remain regarding the resolution of m6A profiling, therapeutic selectivity to avoid unwanted toxicity and biomarker validation for clinical use. This review summarizes the discovery and features of CSCs, highlights the functional role of m6A in GCSCs, and explores diagnostic and therapeutic opportunities while outlining key difficulties for clinical translation.

This review comprehensively examines the dysregulated expression patterns and functions of KIAA1429 in NSCLC, elucidating its m6A-dependent modulation of key downstream effectors (Such as the HOXA1, DAPK3, and BTG2) that orchestrate malignant transformation. We highlight the emerging potential of KIAA1429 as a novel molecular target for precision therapy in NSCLC.

Finally, we constructed a regulatory network linking miRNAs, hub regulators, and 2 downstream target genes. Our study establishes m6A-RPS as a robust tool for prognosis prediction and immune landscape assessment in HCC, offering significant potential to guide personalized therapeutic strategies, particularly immunotherapy selection.

OTUB1 in turn stabilized SLC7A11 expression by deubiquitination. Overexpression of either KIAA1429 or OTUB1 partially reversed the pro-ferroptotic effect induced by FEZF1-AS1 inhibition in MM cells.

Finally, the combined blockade of EV-packaged circTAX1BP1 and TGF-β can effectively disrupt this feedback loop and significantly inhibit tumor progression in a PDX model. Overall, this study provides an in-depth understanding of tumor cell-CAFs crosstalk and new insights into therapeutic targets for CRLM.

Taken together, our findings demonstrate that KIAA1429 promotes ccRCC tumorigenesis by enhancing TMSB10 expression via m6A modification, suggesting it as a potential prognostic biomarker and therapeutic target. However, the lack of clinical validation limits the immediate translational impact of these findings.

KIAA1429 silencing facilitates ferroptosis, thereby delaying OS progression, potentially through modulation of the Nrf2/NQO1 signaling pathway.

Verification of methylation levels indicated that KIAA1429 overexpression resulted in heightened methylation of LINC00958. It was concluded that KIAA1429 diminishes the proliferation, invasion, and tumorigenesis of cancer cells through the methylation of LINC00958.DiscussionThis research provided insights into the role of LINC00958 in oral cancer cells and underscored the impact of methylation, offering a theoretical foundation for improving clinical diagnosis and treatment strategies for oral cancer patients.