RPA3 (Replication Protein A3)

These findings suggest a novel role for ZEB1 in promoting ALT both transcriptionally and post-transcriptionally at multiple levels.

SETD1A promotes breast cancer cell replication through its non-enzymatic role via cyclin K, suggesting that the SETD1A-cyclin K axis could be a potential therapeutic target in breast cancer.

Notably, the expression levels of these three hub genes and the lactylation level of TUBB2A in GBM tissues were significantly higher compared to those in normal tissues. We propose and validate a IQR lactylation screening method that provides potential insights for GBM therapy and an effective framework for developing gene screening models applicable to other diseases and pathogenic mechanisms.

In summary, our results indicate a marked elevation in EXO1 expression levels within gliomas, which correlates strongly with clinical pathological characteristics and unfavorable prognosis. Moreover, EXO1 emerges as a promising candidate biomarker and potential therapeutic target for glioma, likely playing a critical role in mediating immune infiltration within this malignancy.

Functional assays revealed that targeting DDB1 with nitazoxanide significantly downregulated B7-H3 expression, subsequently impairing tumor sphere formation and cell migration in breast CSCs. These findings not only elucidate the complex transcriptional network controlling B7-H3 expression but also open new avenues for developing targeted immunotherapies aimed at disrupting CSC-driven cancer progression.

An innovative signature related to DNA replication was found to be a good prognostic predictor of LUAD. Our findings may provide novel insights into the diagnosis and treatment of LUAD.

Our findings demonstrate that PFKFB3 is crucial for PARPi resistance in OC. Inhibiting PFKFB3 sensitizes HR-proficient OC cells to PARPis by impairing HR repair, leading to increased DNA damage and apoptosis. PFKFB3 represents a promising therapeutic target for overcoming PARPi resistance and improving outcomes in OC patients.

Overall, this study underscores the effectiveness of multi-omics approaches in revealing the molecular mechanisms driving chemotherapy responses in cancer cells. Additionally, this work generates a comprehensive list of molecular alterations that can serve as a foundation for further investigations and inform personalized healthcare strategies to enhance patient outcomes.

These findings highlight tannic acid's ability to induce apoptosis in prostate cancer cells through pro-apoptotic pathways. This study concludes that tannic acid selectively inhibits prostate cancer cell growth.

The growth inhibitory effect of these final shortlisted compounds was examined on a panel of GBM cell lines and compared with temozolomide through the drug sensitivity EC50 values and AUC from the PRISM Repurposing Secondary Screen, and the IC50 values were obtained from GDSC portal...Our results show GSK-2126458/omipalisib, linifanib, drospirenone, eltrombopag, nilotinib, and PD198306 as candidate drugs which can be further evaluated for their anti-tumor potential against GBM. Through this work, we identified repurposed candidate therapeutics against GBM utilizing a GSC inclusive targeting approach, which demonstrated high in vitro efficacy and can prospectively evade drug resistance. These drugs have the potential to be developed as individual or combination therapy to improve GBM outcomes.

In conclusion, our study shows that there is a close relationship between metabolic changes and survival in pGBM. Besides, we established a key miRNAs-LTVSDEGs network for pGBM, which could be the key path in prolonging the life of pGBM patients.