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Last update 08 May 2025

MIR449A

Last update 08 May 2025

Basic Info

Synonyms

hsa-mir-449, hsa-mir-449a, microRNA 449a

+ [3]

Introduction-

Drugs associated with MIR449A

Anti-miRNA-449 (CNRS)

Target

MIR449A

Mechanism

MIR449A inhibitors

Active Org.-

Originator Org.

Centre National de la Recherche Scientifique

Active Indication-

Inactive Indication

Respiration Disorders

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIR449A

100 Translational Medicine associated with MIR449A

0 Patents (Medical) associated with MIR449A

333

Literatures (Medical) associated with MIR449A

01 May 2025·Gene

Molecular Crosstalk by miR-449a and miR-34b in endometrial and ovarian cancer cells in vitro

Article

Author: Hanisha ; Sharma, Indu ; Sharma, Anuradha ; Rana, Akanksha

AIMSEndometrial and ovarian cancers, the sixth and eighth most prevalent cancers in women globally, account for nearly 8% of all new female cancer cases annually. MicroRNAs (miRNAs) have emerged as a promising field in cancer treatment, offering new avenues for targeted therapies and diagnostic tools. Recent miRNA-based cancer research has uncovered various miRNAs commonly dysregulated in cancer and which possess tumor-suppressive functions. These miRNAs influence genes crucial for cellular differentiation, proliferation, apoptosis, and metabolism.MAIN METHODSIn the present study, the researchers investigated the effect of dysregulation of two such miRNAs, miR-449a and miR-34b, on the oncogenes involved in the progression of endometrial and ovarian cancer using the respective RL95-2 and SKOV3 cell lines. The transcriptional gene expression analysis was done by Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR).KEY FINDINGSIt was found that the overexpression of miR-449a and miR-34b downregulated HIF-1α, VEGF, c-Myc, COX-2, and TNF-α while upregulating TP53 in both cancer types. Conversely, inhibiting these miRNAs increased the levels of HIF-1α, VEGF, c-Myc, COX-2, and TNF-α, and decreased TP53. However, co-transfection with both mimic and inhibitor had varying effects.SIGNIFICANCEThe study demonstrated that these miRNAs could influence critical processes such as angiogenesis, proliferation, inflammation, tumorigenesis, and apoptosis in cancer cells, highlighting their potential as therapeutic targets. However, the varied effects observed with the co-transfection of mimics and inhibitors suggest a complex interplay that requires further investigation.

01 Jan 2025·Cell Reports

miR-449a/miR-340 reprogram cell identity and metabolism in fusion-negative rhabdomyosarcoma

Article

Author: Carmeliet, Peter ; Sampaolesi, Maurilio ; Wang, Chao-Chi ; Yedigaryan, Laura ; Planque, Mélanie ; Giarratana, Nefele ; Eelen, Guy ; Garrido, Gabriel Miró ; Koh, Kian Peng ; Uyttebroeck, Anne ; Rinaldi, Gianmarco ; Degreef, Ewoud ; Sassi, Gabriele ; van der Veer, Bernard K ; Marini, Vittoria ; Yustein, Jason T ; Fanzani, Alessandro ; Pozzo, Enrico ; Fendt, Sarah-Maria

Rhabdomyosarcoma (RMS), the most common pediatric soft tissue sarcoma, arises in skeletal muscle and remains in an undifferentiated state due to transcriptional and post-transcriptional regulators. Among its subtypes, fusion-negative RMS (FN-RMS) accounts for the majority of diagnoses in the pediatric population. MicroRNAs (miRNAs) are non-coding RNAs that modulate cell identity via post-transcriptional regulation of messenger RNAs (mRNAs). In this study, we identify miRNAs impacting FN-RMS cell identity, revealing miR-449a and miR-340 as major regulators of the cell cycle and p53 signaling. Through miR-eCLIP technology, we demonstrate that miR-449a and miR-340 directly target transcripts involved in glycolysis and mitochondrial pyruvate transport, inhibiting the mitochondrial pyruvate carrier (MPC) complex. Pharmacological MPC inhibition induces a similar metabolic shift, reducing metastatic potential and leading to cell cycle exit. Overall, miR-449 and miR-340 orchestrate FN-RMS cell identity, positioning MPC inhibition as a strategy to shift FN-RMS cells toward a non-tumorigenic, quiescent state.

03 Dec 2024·JBMR Plus

Differential microRNA expression patterns between TallyHo/JngJ mice and non-diabetic Swiss Webster Random/Jackson mice

Article

Author: Carro Vázquez, David ; Hackl, Matthias ; Wagner, Alisia ; Hofbauer, Lorenz C ; Skalicky, Susanna ; Grillari, Johannes ; Diendorfer, Andreas B ; Emini, Lejla ; Hofbauer, Christine ; Rauner, Martina

AbstractType 2 diabetes mellitus (T2DM) increases the susceptibility of bone fragility. The underlying mechanisms have, however, remained largely unknown. MicroRNAs (miRNAs) are short single-stranded non-coding RNA molecules with utility as biomarkers due to their easy accessibility and stability in bodily fluids. Here, we aimed to use an unbiased approach to identify miRNAs dysregulated in a polygenic mouse model of T2DM. Genome-wide analysis of miRNAs in serum, BM, and bone from the polygenic TallyHo/JngJ (TH) mice, which recapitulate T2DM in humans, was performed. This analysis was compared to the recommended control Swiss Webster Random/Jackson (SWR/J) and a strain-matched non-diabetic control (TH-ND). When comparing TH mice with TH-ND using an adjusted p-value false discovery rate (FDR) cut-off of 0.2 to identify differentially expressed miRNAs, mmu-miR-466i-5p and mmu-miR-1195 were found to be up-regulated in both serum and in BM. Dysregulated miRNAs were not found in bone tissue. When comparing TH-ND mice with SWR/J using the same FDR cut-off, mmu-miR-351-5p, and mmu-miR-322-3p were upregulated in both BM and serum, while mmu-miR-449a-5p and mmu-miR-6240 were downregulated in BM and serum. Dysregulated miRNAs in BM or cortical bone compared to serum between TH-ND mice and SWR/J were investigated for their cell-type enrichment to identify putative donor cells and their gene target networks. Gene target network analysis revealed genes involved in diabetes-related signaling pathways as well as in diabetic bone disease. Cell-type enrichment analysis identified hsa-miR-449a enriched in immune cells, hsa-miR-592 in hepatocytes and endothelial cells, while hsa-miR-424-3p, hsa-miR-1-3p, and hsa-miR-196b-5p were enriched in mesenchymal stem cells and their derived tissues. In conclusion, our comparative miRNA profiling sheds light on differential expression patterns between SWR/J and both subgroups of TH. No differences were observed between TH and TH-ND, suggesting the genetic background of SWR/J may be responsible for the change of dysregulated miRNA.

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MIR449A

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