HNRNPC (Heterogeneous Nuclear Ribonucleoprotein C)

Upon 808 nm laser irradiation, NPs-H-I elicited potent photodynamic therapy (PDT), selectively eliminating HNRNPC-high tumor cells and ITGA1+ myCAFs, which robustly inhibited tumor growth and restored anti-tumor immunity in murine models. Our work not only delineates the HNRNPC-ITGA1 axis as a novel metabolic-immune checkpoint in OSCC but also establishes a versatile and translatable precision medicine platform capable of disrupting this pathway for effective combination therapy.

This study highlights the critical roles of HNRNP family members in LUAD, identifying HNRNPC as a key prognostic biomarker and potential intervention candidate to improve patient outcomes.

Moreover, E2F1 AS activity was evident as cells progress through the cell cycle and during the DNA damage response, and apparent in tumour models. Our results highlight gene networks where transcription and splicing are linked and coordinated by the pRb-E2F pathway, and further establish the widespread influence that pRb, E2F1, and PRMT5 have on regulating biological diversity through RNA splicing control.

Furthermore, tRF-Gly-CCC-012 enhanced HNRNPC protein expression by inhibiting its ubiquitination and degradation, leading to an upregulation of PHGDH and promoting the malignant progression of PC. These findings highlight tRF-Gly-CCC-012 as a viable diagnostic biomarker for PC, providing insights for detection and innovative strategies for clinical intervention.

Using proteomics and transcriptomic profiles, we identified wild-type IDH1 as a crucial metabolic enzyme upregulated in gemcitabine plus cisplatin chemotherapy (GP)-resistant NPC...The DHODH inhibitor BAY2402234 markedly sensitized NPC cells to chemotherapy. Clinically, a prognostic model based on DDR and ferroptosis signatures effectively predicted disease relapse risk post-chemotherapy in NPC. This study links DDR to ferroptosis defense via the IDH1/α-KG/ALKBH5/DHODH axis, suggesting DHODH inhibition as a promising therapeutic strategy to overcome chemoresistance in tumors harboring wild-type IDH1.

Due to their diagnostic, prognostic and predictive value, m6A regulators have emerged as promising biomarkers in gynaecological cancers in recent years. This review highlights the role of m6A regulators and critically evaluates their biomarker and clinical potential in gynaecological cancers.

Additionally, we found that a colon cancer-associated SNP in the POU2AF2/C11orf53 3'UTR creates an ectopic DplUSE site, increasing gene expression in zebrafish gut cells and in a human cell line. We have therefore identified a short 3'UTR motif present in diverse vertebrate genes that controls their expression through conserved RBPs interactions and is implicated in human disease.

Mechanistically, K176la strengthened the binding of HNRNPC with poly-U motifs in p21-activated kinase 6 (PAK6) pre-mRNA, facilitating the expression of the oncogenic isoform PAK6S. Therefore, our study identifies a number of cancer-specific Kla sites spanned on alternative splicing (AS)-related proteins and unravels the significance of HNRNPC K176la in RNA splicing and PC development.

All fusions resulted in transcriptional upregulation of USP6. In this report, we summarize the clinical, radiographic, and histologic presentations of these new cases and describe the associated fusion structures.

Finally, in vivo animal models confirmed that targeted silencing of INTS13 significantly impeded cervical cancer xenograft growth in nude mice, reduced cellular proliferation, and augmented apoptosis, consistently accompanied by a reduction in hnRNPC expression. These findings collectively establish INTS13 as a crucial precancerous gene in cervical cancer, promoting malignant phenotypes primarily through the ZNF384-INTS13-hnRNPC signaling axis.

Furthermore, we discovered that triptolide (TPL), an HNF1A inhibitor, impeded HHIPL2-mediated Sonic Hedgehog signaling activation and NSCLC malignancy. Therefore, our findings not only uncover a previously unrecognized role for HHIPL2 in regulating the Sonic Hedgehog signaling pathway but also highlight a novel HHIPL2/HNRNPC/HNF1A axis as an attractive target for NSCLC therapy.Schematic diagram (created by Figdraw.com) showing that HHIPL2 positively governs Hedgehog signaling to accelerate NSCLC progression via enhancing HNRNPC-mediated HNF1A mRNA stabilization.

Our study constructed a novel signature associated with m6A modifications, which can serve as a promising prognostic indicator for LUAD. These findings may provide valuable insights into diagnosis and therapeutic strategies for patients with LUAD.