MIR199B (MicroRNA 199b)

These alterations reflect both the suppression of upstream Hippo activation and activation of downstream oncogenic effectors across all subtypes. Our findings reveal a conserved Hippo dysregulation program in breast cancer, highlighting subtype-independent Hippo-related genes and their miRNA regulators as potential universal biomarkers and therapeutic targets, complementing subtype-specific treatment strategies.

This miRNA panel outperformed the World Health Organization -endorsed Xpert MTB/RIF assay, effectively identifying early-stage PTB cases without cavity formation. These findings underscore the potential of miRNA-based diagnostics as a non-invasive and highly accurate tool for differentiating PTB from LC in patients with comparable imaging presentations, addressing a critical gap in pulmonary disease management.

Overexpression of miR-199b-5p promotes proliferation, migration, and EMT in lung cancer cells by targeting CCNL1, with its downstream regulatory effects mediated through the Wnt/β-catenin signaling.

This study demonstrates that platelet miRNAs are a superior source for liquid biopsy in LAC compared to exosomal miRNAs. We establish hsa-let-7i-5p as a reliable reference gene and identify platelet hsa-miR-199b-3p as a promising non-invasive biomarker for the differential diagnosis of malignant and benign pulmonary nodules, offering a new avenue for the early detection of lung adenocarcinoma.

Collectively, this ncRNA circuitry regulates T-cadherin across cardiovascular, metabolic, oncogenic, and neurodegenerative conditions. This review integrates both experimentally validated data and in silico predictions to map the ncRNA-CDH13 crosstalk between health and disease, opening new avenues for biomarker discovery and RNA-based therapeutics.

These results may prove an important role of miR-191a expression as a predictor of response to the induction chemotherapy based on cytarabine, even in cases when other risk factors are absent.

Potential miRNA biomarkers, including miR-452-5p, miR-5010-5p, miR-27b-5p, miR-5189-5p, miR-552-5p and miR-199b-5p, were identified. A GC classifier based on these miRNAs was developed, benefiting early detection and population screening.

Urine is a better sample for RIF exo-miRNA detection than blood. Urinary exosomal hsa-miR-143-3p_R+1, hsa-miR-183-5p, hsa-miR-126-3p, mmu-miR-5106_R-4_1ss1AG, hsa-miR-126-5p, and hsa-miR-199b-3p_R-1 are novel liquid biopsy markers for RIF. These DEexo-miRNA may be associated with the occurrence and development of RIF and may participate in specific biological processes by regulating the expression of their target mRNA. Further research may require exploring the specific functions and mechanisms of these miRNAs in RIF, as well as whether they can serve as diagnostic or therapeutic targets for RIF.

The disruption of Scribble localization under hypoxic conditions, but its localization was maintained in miR-199b-5p oral squamous cell carcinoma cell lines and in vivo. These results suggest that Scribble functions as a tumor suppressor marker mediated by miR-199b-5p in oral squamous cell carcinoma.

LINC00665 sponged miR-199b-5p to interact with SERPINE1 expression, resulting in the increase of phosphorylation of AKt, thus participating in the PI3K/AKt pathway. To summarize, LINC00665 facilitated the tumorigenesis and trastuzumab resistance of GC by sponging miR-199b-5p and promoting SERPINE1 expression, which further activated PI3K/AKt signaling; this finding reveals a new mechanism by which LINC00665 modulates tumor development and drug resistance in GC.

In summary, our findings demonstrated that exosomal-specific miR-199b-5p promoted proliferation in distant or neighboring cells via the miR-199b-5p/HIF1AN axis, resulting in enhanced tumor growth.

miR-199b-5p targets solute carrier transporters (SLC1A2/EAAT2 in astrocytes and SLC38A2/SNAT2 and SLC16A7/MCT2 in neurons) to hijack the neuron-astrocyte metabolic coupling, leading to extracellular retention of these metabolites and promoting cancer cell growth. Our findings reveal a mechanism through which cancer cells of a non-brain origin reprogram neural metabolism to fuel brain metastases.