DNAJC12 (DnaJ Heat Shock Protein Family (Hsp40) Member C12)

Our study identified 5 previously unreported genes as potential diagnostic biomarkers and therapeutic targets for HCC. These findings provide a new perspective for the molecular characterization and clinical management of hepatocellular carcinoma.

Silencing FGL1 promotes prostate cancer cell apoptosis and inhibits EMT progression. FGL1 may be an independent prognostic marker and therapeutic target in PCa.

Overall, our study demonstrated that heat shock protein genes were significantly linked to glioma patient prognosis. Additionally, we observed that HSP90B1 had a significant relationship with M2 macrophage infiltration and potentially regulated LDHA level in glioma.

Using IHC analysis, we showed that low DNAJC12 protein-level expression is also associated with a worse prognosis in patients with all subtypes of BC and patients with Luminal BC, and its expression is significantly different between patients with different tumor size classifications (T1/T2 vs T3/T4; P = .013) or with different lymph node involvement (N0 vs N+; P = .005). Our findings suggested a potential role for DNAJC12 as a prognostic and predictive biomarker for BC.

This study sheds light on the significant impact of HBCD on gene and miRNA expression in prostate cancer, emphasizing the potential of the identified hub genes and miRNAs as prognostic biomarkers and therapeutic targets. By elucidating the pathways and regulatory networks influenced by HBCD, the findings provide a foundation for developing strategies to mitigate its carcinogenic effects and improve outcomes for prostate cancer patients.

Furthermore, we showed that inhibiting glycolysis, reducing H4K5la, or targeting COL1A1 can mitigate the invasive behavior of NB cells. These findings reveal a critical link between metabolic reprogramming and epigenetic modifications in the context of NB progression, suggesting that H4K5la could serve as a novel diagnostic and prognostic marker, and shed light on identifying new therapeutic targets within metabolic pathways for the treatment of this aggressive pediatric cancer.

S100A8/A9 may be a promising marker for the diagnostic and prognostic assessment of the HNSCC patients. Based on these insights, we have devised a new classification model for HNSCC, which has the potential to enhance the management and personalized treatment of HNSCC patients. The model should also be further optimized through the expansion of sample size and implemented experimental studies in future research.

DNAJC12 expression is closely linked to chemoresistance in BC. The DNAJC12-HSP70-AKT signaling axis is crucial in mediating resistance to chemotherapy by suppressing DOX-induced ferroptosis and apoptosis. Our findings suggest that targeting AKT and HSP70 activities may offer new therapeutic strategies to overcome chemoresistance in BC.

Finally, DNAJC12 silencing hampered tumor growth of RC in vivo. In summary, this study highlighted a key player of DNAJC12 in modulating the malignant biological progression of RC via DNAJC12/HSPA4 axis, displaying a potential therapeutic target for RC.