Our findings suggest that NAT10-mediated acetylation of JARID2 mRNA up-regulates its protein levels, thereby promoting stemness and contributing to the malignancy of GBM. Targeting this NAT10-JARID2 axis may represent a novel therapeutic approach for treatment of GBM.

Taken together, the study has confirmed that JARID2 acts as a tumor suppressor, the downregulation of which promotes OSCC progression by regulating Epithelial-to-Mesenchymal Transition (EMT). The online version contains supplementary material available at 10.1007/s13205-024-04163-8.

Knockdown of JARID2 inhibited tumor growth and cell stemness in mice but was alleviated by concurrent overexpression of NFYA. NFYA promotes TNBC cell stemness by upregulating JARID2 expression and regulating the PI3K/AKT signaling pathway, suggesting JARID2 as a potential target for innovating drugs that target TNBC stem cells.

Our study indicates that JARID2 is a novel prognostic biomarker and potential therapeutic target for OSCC.

VPA downregulates the expression level of miR-155 by increasing the methylation level of the miR-155 promoter, suggesting that the miR-155/JARID2 axis is implicated in VPA inhibition of glioma cell viability and enhancement of glioma cell apoptosis. This study demonstrates a new mechanism of VPA treatment of gliomas by affecting the miR-155/JARID2 axis, which could be regarded as a new strategy for the prevention and treatment of glioma.

Our data indicated that JARID2 promoted breast tumorigenesis and development, confirming JARID2 as a target for cancer treatment.

Furthermore, our findings indicated that JARID2 promotes the proliferation of SKOV3 cells, suggesting its oncogenic role in OC. JARID2, potentially regulated by the PKD1P6/miR-424-5p/JARID2 axis, represents a potential novel biomarker for OC.

Accordingly, the opposite results were obtainedwhen JARID2 was downregulated. Furthermore, JARID2 promoted the invasion and migration ability of Ishikawa cells.

Integrating analysis of the RNA and DNA binding profiles suggests EZH2 and JARID2 shift their binding ability from DNA to RNA in HepG2 cells to promote cancer development in HCC. Our study provided a comprehensive and distinct binding profile on RNAs and DNAs of EZH2 and JARID2 in liver cancer cell lines, suggesting their potential novel functional manners to promote HCC development.

Accordingly, PALI1 and G9A drive PCa cell proliferation and invasion in vitro and xenograft tumor growth in vivo. Collectively, our study shows that PALI1 harnesses two central epigenetic mechanisms to suppress cellular differentiation and promote tumorigenesis, which can be targeted by dual EZH2 and G9A inhibition.

Moreover, the results of qRT-PCR and western blot showed that LINC00852 could regulate the expression of JARID2 through miR-29a-3p induction. In summary, we demonstrated that LINC00852 played a key role in promoting the prostate cancer, and LINC00852/miR-29a-3p/JARID2 axis could be used as a target for prostate cancer treatment.