NFIC (Nuclear Factor I C)

ECRG4 inhibits breast cancer progression by positively regulating NFIC/PTEN to suppress the SHP2/PI3K/SP1 signaling pathway. Targeting this signaling axis may provide a new strategy for breast cancer treatment.

These findings offer preliminary clues for future risankizumab-based combination strategies in psoriasis.

First of all, our study shows that OP could induce the unbalanced hematopoiesis and enhances the myeloid-biased hematopoiesis. Secondly, OP mice enriched subsets of HSPCs were identified and characterized with enhanced chromatin remodeling, reduced differentiation and resistance to apoptosis. Finally, this study demonstrate that Brd4 regulated gene programs endow the myeloid-biased subsets of HSPCs with tumor cell-like characters in OP mice, which may increase the incidence of the leukemic evolution. This study sheds light on the importance for the prevention of myeloid leukemogenesis in human with OP.

NFIC mediates DEPTOR transcription to repress mTOR signaling, thereby hindering OSCC progression by suppressing cell proliferation, glycolytic activity, and CD8+ T cell-related immune escape.

Recent reports have indicated that the minor allele of the nuclear transcription factor I/B (NFIB), rs28379954 T>C, affects the metabolism of risperidone and clozapine, which are mediated by CYP2D6 and CYP1A2, respectively. First, we reanalyzed the association between rs28379954 T>C and CYP2D6 activity in three independent cohorts exposed to CYP2D6 substrates (propafenone, tamoxifen, and sparteine) which revealed no association...We identified significant downregulation of several metabolic pathways related to hepatic functionality, PPAR signaling, and drug metabolism for NFIB, NFIC, and NFIX, whereas pathways associated with cancer biology were significantly induced. In summary our findings provide further insight into hepatic CYP regulation via the NFI network with implications for the understanding of interindividual variability of drug metabolism.

The changes identified indicate a complex reprogramming of transcriptional activity affecting cell cycle processes, DNA repair, metabolism, and the epithelial-mesenchymal transition. The findings expand our understanding of the molecular mechanisms of trastuzumab resistance and open prospects for the development of novel therapeutic strategies to overcome drug resistance in HER2-positive breast cancer.

Furthermore, overexpression of ID1 promoted the progression of esophageal cancer, and the expression of ID1 in human cancerous tissues was significantly higher than that in peritumoral tissues. ID1 promotes the progression of esophageal cancer by inducing proliferation and immune suppression through regulation of the PTEN/YAP/Galectin-3 signaling pathway.

Stool Fibrinogen, MMP-8, MMP-9, PGRP-S, Haptoglobin, and Myeloperoxidase emerge as promising biomarkers for distinguishing CRC/advanced adenomas/healthy stools, meeting or outperforming current yardsticks.

Genome-wide association studies have identified RGPR-p117/SEC16B as an obesity-associated gene, suggesting RGPR-p117's involvement in lipid metabolism in obesity. This review discusses RGPR-p117's advanced role in regulating cellular processes, such as cell proliferation and lipid metabolism, as well as its relationship with obesity.

The overexpression of NFIC and COL4A5 was closely related to the tumor, node, metastases stage of NPC patients. Collectively, our results suggest that NFIC transcriptionally activates COL4A5 and upregulates its expression, which mediates DDR1/Akt signaling and promotes the malignant behavior of NPC cells, leading to NPC progression.

This study provides a comprehensive single-cell resolution map of LUAD progression, highlighting epithelial-driven regulatory programs and dynamic intercellular communication within the TME. Our findings uncover novel molecular markers and regulatory mechanisms with potential prognostic and therapeutic value for more precise treatment.

NFIC inhibited the migration and proliferation of SKOV3 cells, while TBX2 promoted it; NFIC functioned through TGFβ1 and PTEN, and their inhibition promoted the migration and proliferation of SKOV3 cells. NFIC inhibits the progression of epithelial ovarian cancer by regulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 to suppress the TBX2/MMPs signaling pathway.