MIR623 (MicroRNA 623)

Sequencing and bioinformatics analysis revealed these microRNAs likely regulate key ROS-associated genes and pathways, including FN1, EZR, TRX2, and MAP2K1. Their dysregulation suggests a role in tumor progression, underscoring the need to further investigate microRNA-mediated gene regulation under space-like conditions to better understand the long-term health risks associated with extended space travel.

Our study suggests candidate molecular mechanisms linking periodontitis to prostate cancer, highlighting potential compounds targeting both diseases. These findings provide a foundation for guiding future basic and clinical research.

Additionally, the PI3K-Akt, p53, Ras, and Rap1 signaling pathways were demonstrated to be the key pathways, whereas CDK6, PIK3CB, and KRAS were found to be directly functional target genes. Our findings imply that miRNA-6236-p5_4 can act as both a molecular diagnostic for the clinical identification and prognosis of EC and a tumor suppressor in AA against EC.

Based on our results, the transcriptome profile of ARDS patients would be a valuable source for understanding molecular mechanisms of host response and developing clinical guidance on anti-inflammatory medication.

RP11-89 and miR-623 showed no direct role in each other's expression. RP11-89 suppressed the role of miR-623 in downregulating cyclin D1 and GBM cell proliferation. Therefore, miR-623 may link lncRNA RP11-89 and cyclin D1 to regulate the proliferation of GBM cells.

Our study elucidates, for the first time, the crucial role of miR-623 as MMP1 direct regulator in BCBMC and sheds light on miR-623 as a novel therapeutic target that can be exploited to predict and prevent brain metastasis in TNBC. Importantly, the presents study helps in unraveling a brain metastasis-specific microRNA signature in TNBC that can be used as a guide to personalized metastasis prediction and preventive approach with better therapeutic outcome.

This study reveals the network relationship between colon cancer exosome-derived miRNA and targeted mRNA. It deepens our understanding of new molecular mechanisms and pathways that may play a role in the occurrence and metastasis of colon cancer.

Dysregulated miRNA and its target genes illustrate the physiological role of miRNAs in fibrosis. Understanding the miRNA-mediated fibrotic signaling, and targetting the specific miRNA-target gene interaction might provide relevant cues to ameliorate the fibrotic disease.