HNRNPD (Heterogeneous Nuclear Ribonucleoprotein D)

Moreover, cisplatin in combination with silencing of hnRPD expression, significantly induces apoptosis in cisplatin-resistant OC cells through regulation of OC cell metabolism. Therefore, our data provide evidence that hnRPD could represent an innovative prognostic indicator for OC and may be an attractive therapeutic target for improving clinical outcomes in OC treatment.

ZEB1 interacted with the E-box motif in the GPX4 promoter, suppressing GPX4 transcription and thereby promoting ferroptosis. In conclusion, RBMS3-AS3, epigenetically downregulated by ALKBH5, facilitates LUAD progression by inhibiting ferroptosis via the HNRNPDL/ZEB1/GPX4 axis, and may serve as a novel therapeutic target for LUAD.

This leads to decreased stability of ZEB2 mRNA, inhibition of the epithelial-mesenchymal transition, and consequent suppression of NPC metastasis. Overall, this study reveals a critical role of circUBAP2(9,12) in NPC progression and highlights its potential as a therapeutic target for metastatic NPC.

Together, our findings delineate a previously unrecognized SELENBP1-p21-AUF1-MMP2 axis that links SELENBP1-mediated invasion suppression to post-transcriptional control of extracellular matrix remodeling. This study highlights SELENBP1 as a multifunctional tumor suppressor and suggests that restoring this pathway may offer therapeutic opportunities in invasive cancers.

Protein stability analysis confirmed their destabilizing effects, while functional enrichment highlighted their involvement in key pathways driving tumorigenesis. This study identified 11 key DEGs harboring potentially pathogenic novel missense variants, highlighting vulnerabilities for precision-targeted therapies in EC.

Our findings reveal a novel hsa_circ_0038737/IGF2BP3/DNPH1 axis driving PARPi resistance in CRPC, offering promising potential biomarkers and therapeutic targets to overcome resistance and improve treatment outcomes in advanced prostate cancer.

AUF1 and HIF-1α may work in concert to accelerate the development of PTC. And they may be useful biomarkers for PTC and lymph node metastases.

Our study highlights hnRNPD as a major contributor to gastric carcinogenesis. The knockdown of hnRNPD hinders gastric cancer growth by directly interacting with TXNIP, promoting its expression, and inducing oxidative stress. These findings suggest that hnRNPD may serve as a valuable target for the treatment of gastric cancer.

Together, these mechanisms form a complex and intricate post-transcriptional regulatory network that governs MAT activity in physiological and pathological states. This review examines emerging insights into MAT post-transcriptional regulation, focusing on its implications for liver cancer, and opens new avenues for developing therapies that target these regulatory mechanisms.

This presents a novel potential target for the targeted therapy of NSCLC. Our research demonstrated that HNRNPD facilitates vasculogenic mimicry development and tumor progression in NSCLC via activating the SIRT1/PGC-1α pathway, offering a novel approach for targeted therapy in NSCLC.

PP4C is involved in hepatic lipid metabolism by regulating AUF1 phosphorylation under different oxygen concentrations. PP4C might be a promising target for treating hepatic lipid accumulation.

o8G-modified circPLCE1 inhibits lung cancer progression through CMA to inhibit macroautophagy and alter cell fate. This study provides not only a new theoretical basis for elucidating the molecular mechanism of lung cancer progression but also potential targets for lung cancer treatment.