MIR193B (MicroRNA 193b)

AML with HOXB3 hypomethylation usually has unique genetic patterns such as a normal karyotype, cytogenetic/molecular-intermediate risk, and mutations in FLT3-ITD, NPM1 and DNMT3A. Despite these associations, HOXB3 hypomethylation may serve as an independent prognostic biomarker for AML.

However, miR-193b does not have a single, unified function; instead, its role is highly context-dependent, acting as either a protective molecule or a pathogenic driver depending on the specific tissue and disease. This review aims to consolidate the current updates on the role of miR-193b, detailing its molecular mechanisms, validated target genes, and its burgeoning potential as a diagnostic biomarker and therapeutic agent in cancer and other pathological conditions.

MiR-193b-3p targets and downregulates HPRT1. Overexpression of HPRT1 reverses the suppressive effects caused by JHDM1D-AS1 depletion on CRC cell malignancy. In conclusion, JHDM1D-AS1 promotes CRC cell proliferation, metastasis, invasion and tumor development by upregulating HPRT1 expression via miR-193b-3p.

This integrative model effectively predicted 1-, 3-, and 5-year survival probabilities, thereby stratifying patients into distinct risk categories for enhanced clinical decision-making and personalized follow-up strategies. This research validates the diagnostic and prognostic utility of exosomal miRNA models in MM, emphasizing their discriminative and predictive capabilities.

We also discuss miRNAs (such as miR-519a-3p, let-7e, miR-216b), which affect responses to OvCa therapy by targeting PARP1 (Poly(ADP-Ribose) Polymerase-1). Finally, we also discuss why, despite the identification of multiple miRNAs capable of regulating DNA repair genes, as well as those involved in the response to therapy, no miRNA-based drugs have been approved for OvCa treatment in clinics.

The diagnostic model achieved an AUC of 0.956, a sensitivity of 94%, and a specificity of 93% in the training cohort and an AUC of 0.985, a sensitivity of 86%, and a specificity of 97% in the validation cohort. Our findings demonstrates that plasma sEV miRNA exhibits a highly discriminative biomarker for distinguishing NCs group from early malignant lesions, making it a promising tool for auxiliary detection of early-stage LC.

We investigated whether angiogenesis-related microRNAs (miRNAs) predict survival in patients with pleural mesothelioma (PM) treated with bevacizumab plus pemetrexed-platinum chemotherapy in the Mesothelioma Avastin Cisplatin Pemetrexed Study ('MAPS', NCT00651456) phase 3 trial phase III trial (NCT00651456). Additionally, low expression of miR-155-5p, miR-29c-5p, miR-132-3p, and miR-100-5p showed independent predictive value for improved survival in the bevacizumab plus chemotherapy arm. Thus, a simple qRT-PCR assay of these four miRNAs may help identifying PM patients most likely to benefit from bevacizumab.

Also, RNA-seq results suggested an increased sensitivity of pSS1 cells to immunostimulation. These results reflect current pathobiology aspects, confirming the relevance of immortalized salivary gland epithelial cell lines.

Injection of AgomiR-193b-3p into mice bearing ESCA xenografts impeded tumor growth. These findings underscore the critical role of the miR-193b-3p/RSF1 axis in esophageal cancer progression.

Additionally, miR-193b-3p increased IGF-1R/Akt/MDM2/p53 signaling-mediated autophagy induction, which in turn facilitated increased HBV post-transcriptional activity. Collectively, hepatocyte-enriched miR-193b-3p exerts a proviral effect on HBV replication through dual synergistic mechanisms, offering novel insights into its role in HBV replication and potential therapeutic implications in CHB infection.

Our study suggests that the interaction between miR-193b-3p, TGFβ2, and the acidic tumor microenvironment promotes cancer EMT change. Understanding these interactions may not only enhance our biological comprehension of cancer, but also pave the way for the development of targeted therapies to inhibit cancer metastasis.

This study is the first to uncover a novel regulatory pathway where c-Jun acts as a transcriptional repressor of miR-193b-3p, leading to PRNP upregulation, which promotes lung cancer migration and invasion. This previously unrecognized c-Jun-miR-193b-3p-PrPc axis also provides valuable insights for the potential development of new therapeutic strategies against lung cancer metastasis through RNA-targeting technology.