PCBP2 (Poly(RC) Binding Protein 2)

The ELK3-SERPINE1-PCBP2 axis promotes GEF resistance in lung cancer by inhibiting ferroptosis, providing a potential new therapeutic strategy for overcoming chemoresistance.

Benefiting from its deep-tissue photoactivation, high catalytic efficiency, and multi-target synergistic mechanisms, ENCF achieved potent tumor suppression with selective accumulation at metastatic sites in a bone metastasis model. Collectively, this study establishes a multi-pronged therapeutic strategy via "CO release-autophagy enhancement-ferroptosis activation," offering a promising and innovative approach for the precise treatment of bone metastases.

ID is closely associated with aggressive tumor biology, suboptimal response to neoadjuvant therapy, and impaired postoperative recovery. Dysregulation of iron homeostasis and ferroptosis pathways in ID patients may contribute to CRC progression. These findings highlight ID as a potential biomarker for risk stratification and suggest that targeting iron metabolism could improve therapeutic outcomes in CRC management.

We conclude that PCBP2 is a target of fasting and is involved in cell migration/invasion and glycolysis through the negative regulation of ANGPTL4 in GBC. PCBP2 represents a potential therapeutic target for GBC.

PCBP2-mediated upregulation of PARP1 enhanced DNA repair activity, contributing to olaparib resistance. Together, these findings unveil a mechanism by which PCBP2 upregulates PARP1 to promote olaparib resistance in BRCA-mutated breast cancer, indicating that targeting this pathway could represent a therapeutic strategy to overcome PARPi resistance in breast cancer.

Furthermore, it explores the intricate molecular pathways implicated in cancer progression where PCBP2 plays a significant role. Additionally, this discourse encapsulates the prospective clinical utilities of PCBP2, spanning diagnosis, therapeutic modalities, and prognostication in the realm of gastrointestinal cancers.

Additionally, depletion of PCBP2 impaired the EGFR-driven tumor angiogenesis by inhibiting the secretion of pro-angiogenic miRNAs through sEVs. EGFR boosts PCBP2 expression via transcriptional regulation, which then promotes the loading of specific miRNAs into sEVs by binding to the "GGGU" motif, thereby driving tumor angiogenesis.

Actinomycin D assay was performed to investigate the effect of PCBP2 depletion on TROAP mRNA stabilization...Our study demonstrated that PCBP2 stabilized TROAP to promote the malignant progression of gastric cancer. Targeting PCBP2 and its downstream target TROAP may provide a novel therapeutic strategy for the treatment of gastric cancer.

Silencing of circ_0005397 reduced tumor growth by enhancing erastin-induced ferroptosis in vivo. EIF4A3-induced circ_0005397 inhibited erastin-induced ferroptosis in pancreatic cancer by promoting PCBP2 expression through KAT6A and H3K9ac.

We established a novel DRGI-based prognostic and diagnostic model for HNSC, exploring its tumor immune microenvironment implications, and offering valuable insights for future research and clinical trials.

Treatment with LY294002, an inhibitor of the PI3K/AKT signaling pathway, also reversed the effects of PCBP2 in melanoma cells. Furthermore, our results suggest that miR-5195-3p inhibits the activation of the PI3K/AKT signaling pathway in melanoma by inhibiting PCBP2. In conclusion, our research has identified the miR-5195-3p targeting of the PCBP2-mediated PI3K/AKT signaling pathway as a potential therapeutic target for melanoma treatment.

METTL3-mediated m6A modification increases PCBP2 stability. Along the cGAS-STING signal pathway, PCBP2 decreased the apoptosis that oxidative stress-induced glioma caused, which might be a potential target to suppress oxidative stress-induced apoptosis of glioma.