KHDRBS3 (KH RNA Binding Domain Containing, Signal Transduction Associated 3)

Notably, 25(OH)D exhibited a synergistic effect with GSK-J4, a specific inhibitor of KDM6A, in suppressing breast cancer cell growth. Collectively, our findings uncover a novel anticancer mechanism of 25(OH)D, highlight the critical role of KDM6A Δexon13 in breast cancer progression, and provide further evidence supporting the correction of 25(OH)D deficiency in breast cancer patients.

These findings uncover novel roles for KHDRBS2 and KHDRBS3 in PCa progression, with KHDRBS2 identified as a potential key regulator of AR-V7 expression. Our results provide new insights into AR splice variant regulation and highlight potential therapeutic targets for PCa treatment.

qRT-PCR and Western blot confirmed PTPRF, ULK1, TGM3, and CRABP2 were upregulated at both the mRNA and protein levels. These findings indicate that the Treg-related signature serves as robust prognostic biomarkers and may guide personalized immunotherapy in SCKM.

KHDRBS3-mediated upregulation of circ_0024107 in gastric cancer cells and GC-MSCs synergistically enhances gastric cancer progression. This elucidates novel molecular interactions between GC-MSCs and gastric cancer cells, thereby presenting a promising therapeutic target for effectively mitigating gastric cancer metastasis.

KHDRBS3 also predicted the possibility of not responding to taxane-based therapy. Finally using the computational molecular docking and molecular dynamic simulation over a time period of 60 ns we screened a steroidal lactone i.e. Withaferin A, that showed strong binding affinity towards the active site of KHDRBS3 and also qualified drug-likeness properties essential to be utilized for therapeutic purposes in future.

Our findings indicated that circFOXP1-encoded p196 plays a role as a tumor promoter, contributing to the malignant progression of HCC. Targeting the circFOXP1/p196-KHDRBS3-ULK1 axis presents a promising therapeutic strategy for HCC, with potential applications in biomarker development and combination therapies.

Furthermore, we explored the differences between high- and low-risk groups through mutation and immune infiltration analyses. Lastly, we investigated immunotherapy responses and drug sensitivities between risk groups, providing novel therapeutic insights for liver cancer.

Our study highlights KHDRBS3 as an essential proviral host factor that is key to the successful completion of KSHV lytic replication and suggests its novel function in viral lytic gene transcription during KSHV reactivation. Taken together, these findings reveal a previously unrecognized role for the miR-31-5p/KHDRBS3 axis in regulating the KSHV latency-lytic replication switch and provide insights into gene expression regulation of lytic KSHV, which may be leveraged for lytic cycle-targeted therapeutic strategies against KSHV-associated malignancies.

Using large SPTB families, we identified shared chromosomal regions (8q24.23 and 12q21.1-q21.2), providing evidence for inherited (segregating) risk loci in SPTB etiology. Further investigation into genes in SPTB etiology, including functional validation may provide avenues for novel therapeutic development and guide efforts for SPTB prevention to prolong pregnancy and improve outcomes.

There is a high demand to develop biomarkers that would help the diagnosis and prognosis of prostate cancer. Tissue biomarkers are of particular interest since immunohistochemistry remains a cheap, reliable method that is widely available in pathology departments. These results demonstrate that testing biomarkers in a cohort consistent with the current diagnostic pathway is crucial to identifying biomarker with potential clinical utility.

Collectively, our results highlight KHDRBS3 as a novel factor associated with self-renewal of glioblastoma stem-like cells and TMZ resistance. As a consequence, targeting KHDRBS3 may help eradicate glioblastoma stem-like cells.

TPT1-AS1 promotes OC progression by inhibiting ferroptosis and upregulating CREB1, forming a regulatory axis with KHDRBS3. These findings highlight the regulatory network involving lncRNAs, RBPs, and transcription factors in cancer progression.