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BIOMARKER:

miR-139-5p expression

i
Other names: MIR139, MicroRNA 139, Hsa-MiR-139-3p, Hsa-MiR-139-5p, MIMAT0004552, MIMAT0000250, Hsa-MiR-139, MiR139-3p, MI0000261, MiR-139, MiRN139, RF00703, MiR139
Entrez ID:
25d
MCPIP1 modulates the miRNA‒mRNA landscape in keratinocyte carcinomas. (PubMed, J Exp Clin Cancer Res)
Loss of MCPIP1 modulates the expression profiles of 33 miRNAs in chemically induced Mcpip1eKO papillomas, and these changes directly affect the miRNA‒mRNA network and the modulation of pathways and processes related to carcinogenesis.
Journal
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MIR139 (MicroRNA 139) • MIR223 (MicroRNA 223)
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miR-139-5p expression
7ms
The novel circ_0004674/miR-139-5p/ZBTB2 regulatory cascade inhibits the development of oral squamous cell carcinoma. (PubMed, Head Neck)
Our findings uncover a novel regulatory cascade, the circ_0004674/miR-139-5p/ZBTB2 axis, with the ability to affect OSCC development in vitro and in vivo, providing a potential opportunity for development of OSCC therapy.
Journal
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MIR139 (MicroRNA 139)
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miR-139-5p expression
7ms
Micro-RNAs With Prognostic Significance in Gallbladder Cancer: A Systematic Review and Meta-Analysis. (PubMed, Cureus)
In conclusion, specific miRNAs exhibit prognostic significance in GBC, with potential implications for patient stratification and targeted therapeutic interventions. However, due to the heterogeneity among studies, these findings should be interpreted cautiously and validated in larger cohorts.
Retrospective data • Review • Journal
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MIR7 (MicroRNA 7) • MIR139 (MicroRNA 139) • MIR141 (MicroRNA 141) • MIR335 (MicroRNA 335) • MIR92B (MicroRNA 92b) • MIR204 (MicroRNA 204) • MIR20A (MicroRNA 20a)
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miR-139-5p expression
8ms
GALNT2 targeted by miR-139-5p promotes proliferation of clear cell renal cell carcinoma via inhibition of LATS2 activation. (PubMed, Discov Oncol)
Based on our experiments, miR-139-5p overexpression inhibited RCC proliferation, and this phenotype was rescued by GALNT2 overexpression. Given these evidences, the miR-139-5p-GALNT2-LATS2 axis is critical for RCC proliferation, and it is an excellent candidate for a new therapeutic target in ccRCC.
Journal
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LATS2 (Large Tumor Suppressor Kinase 2) • MIR139 (MicroRNA 139) • GALNT2 (Polypeptide N-Acetylgalactosaminyltransferase 2)
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miR-139-5p expression
9ms
Activation of Notch1-GATA3 pathway in asthma bronchial epithelial cells induced by acute PM2.5 exposure and the potential protective role of microRNA-139-5p. (PubMed, J Asthma)
Acute PM2.5 exposure can activate Notch1-GATA3 pathway in asthma bronchial epithelial cells model, which might be involved in PM2.5-induced asthma exacerbation. miR-139-5p has a potential protective role of inhibiting PM2.5-induced asthma airway inflammation by targeting Notch1.
Journal
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NOTCH1 (Notch 1) • GATA3 (GATA binding protein 3) • MIR139 (MicroRNA 139)
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NOTCH1 expression • miR-139-5p expression
10ms
Noval ceRNA axis-mediated high expression of TOP2A correlates with poor prognosis and tumor immune infiltration of hepatocellular carcinoma. (PubMed, Transl Cancer Res)
Additionally, TOP2A influences the development of HCC by affecting TIICs and immune checkpoints. A nomogram constructed using the three lncRNAs and clinicopathological features has good clinical utility.
Journal
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TOP2A (DNA topoisomerase 2-alpha) • MIR139 (MicroRNA 139)
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miR-139-5p expression • TOP2A expression
12ms
The Signaling Pathways Enriched in High-Risk AML Patients Revealed By the Integrative miRNA-mRNA Analysis - Pilot Study (ASH 2023)
In FLT3 mutated pts standard induction/consolidation therapy was enriched with midostaurin. Low intensity treatment consisted of azacitidine (1 pts), low dose Ara-C (LDAra-C, 2 pts) and LDAra-C + cladribine (1 pts)...ConclusionsOur preliminary results indicate the signaling pathways disturbed in high-risk AML patients. The miR-125b-5p, miR-15a-5p as well as the TEK and SPP1 gene expression may possibly act as biomarkers in patients with de novo AML.
Clinical
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FLT3 (Fms-related tyrosine kinase 3) • NOTCH1 (Notch 1) • FGFR (Fibroblast Growth Factor Receptor) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • SPP1 (Secreted Phosphoprotein 1) • CXCL12 (C-X-C Motif Chemokine Ligand 12) • MIR34A (MicroRNA 34a-5p) • MIR199B (MicroRNA 199b) • JAG1 (Jagged Canonical Notch Ligand 1) • MIR139 (MicroRNA 139) • MIR424 (MicroRNA 424) • SLIT2 (Slit Guidance Ligand 2) • MIR15A (MicroRNA 15a) • MIR181A1 (MicroRNA 181a-1) • MIR204 (MicroRNA 204) • MIR218 (MicroRNA 218) • PPIA (Peptidylprolyl Isomerase A)
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FLT3 mutation • miR-139-5p expression
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cytarabine • azacitidine • Rydapt (midostaurin) • cladribine
12ms
EZH2-H3K27me3-mediated silencing of mir-139-5p inhibits cellular senescence in hepatocellular carcinoma by activating TOP2A. (PubMed, J Exp Clin Cancer Res)
Our study revealed the role of the EZH2/miR-139-5p/TOP2A axis in regulating cellular senescence and cell proliferation in HCC, enriching the molecular mechanisms of EZH2-mediated epigenetic regulation in HCC. Therefore, our results provide insight into the therapeutic potential of targeting EZH2 to induce cellular senescence and then destroy senescent cells for HCC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • TOP2A (DNA topoisomerase 2-alpha) • MIR139 (MicroRNA 139)
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TOP2A overexpression • EZH2 overexpression • miR-139-5p expression • TOP2A expression
1year
VALIDATION AND ASSESSMENT FEASIBILITY OF HSA‐MIR‐139‐5P EXPRESSION AS A PROGNOSTIC MARKER IN THYROID CANCER (ATA 2023)
Our results confirm the value of miR139‐expression as a prognostic marker in thyroid cancer and underscores the clinical utility of in situ miR139‐expression assessment in diagnostic biopsies.
TERT (Telomerase Reverse Transcriptase) • MIR139 (MicroRNA 139)
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TERT mutation • KIT expression • TERT promoter mutation • miR-139-5p expression
1year
MicroRNA-139-5p suppresses non-small cell lung cancer progression by targeting ATAD2. (PubMed, Pathol Res Pract)
MiR-139-5p was a tumor suppressor in NSCLC by regulating the oncogene ATAD2 and β-catenin signaling. Our study provides a promising target for cancer treatment.
Journal
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MIR139 (MicroRNA 139) • ATAD2 (ATPase Family AAA Domain Containing 2)
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miR-139-5p expression
over1year
Androgen receptor suppresses lung cancer invasion and increases cisplatin response via decreasing TPD52 expression. (PubMed, Int J Biol Sci)
Collectively, the results from our study suggest that AR can suppress lung cancer cell invasion and increase DDP response by modulating the circ-SLCO1B7/miR-139-5p/TPD52 signaling pathway. Targeting this novel signaling pathway may be a new therapeutic strategy to effectively constrain NSCLC development.
Journal
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AR (Androgen receptor) • MIR139 (MicroRNA 139)
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miR-139-5p expression
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cisplatin
over1year
LncRNA AC012360.1 facilitates growth and metastasis by regulating the miR-139-5p/LPCAT1 axis in hepatocellular carcinoma. (PubMed, Environ Toxicol)
Furthermore, miR-139-5p silencing partially mitigated the role of AC012360.1 knockdown, while LPCAT1 knockdown partially abolished the tumor-promoting effect of AC012360.1 overexpression. In conclusion, AC012360.1 exhibited its oncogenic function in HCC through sponging miR-139-5p and upregulating LPCAT1 expression.
Journal
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MIR139 (MicroRNA 139) • LPCAT1 (Lysophosphatidylcholine Acyltransferase 1)
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miR-139-5p expression
over1year
Tumor-suppressive role of miR-139-5p in angiogenesis and tumorigenesis of ovarian cancer: Based on GEO microarray analysis and experimental validation. (PubMed, Cell Signal)
The miR-139-5p/SOX4/TMEM2 axis also reduced VEGF expression and angiogenesis, which might curtail OC growth in vivo. Collectively, miR-139-5p represses VEGF expression and angiogenesis by targeting the transcription factor SOX4 and down-regulating TMEM2 expression, thereby impeding OC tumorigenesis.
Journal
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MIR139 (MicroRNA 139) • SOX4 (SRY-Box Transcription Factor 4)
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VEGFA expression • miR-139-5p expression
over1year
FTO-stabilized miR-139-5p targets ZNF217 to suppress prostate cancer cell malignancies by inactivating the PI3K/Akt/mTOR signal pathway. (PubMed, Arch Biochem Biophys)
Finally, our rescuing experiments confirmed that overexpressed FTO-induced tumor-suppressing effects on PC cells were abrogated by miR-139-5p ablation and ZNF217 overexpression. Collectively, this study firstly validated that FTO exerted its anti-tumor effects in PC through regulating the miR-139-5p/ZNF217 axis in a m6A-dependent manner, providing novel biomarkers for the advancement of anti-cancer agents for PC treatment.
Journal
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ZNF217 (Zinc Finger Protein 217) • FTO (Alpha-Ketoglutarate-Dependent Dioxygenase FTO) • MIR139 (MicroRNA 139)
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FTO expression • miR-139-5p expression • FTO overexpression
over1year
Paeonol inhibits melanoma growth by targeting PD1 through upregulation of miR-139-5p. (PubMed, Biochem Biophys Res Commun)
Dual-luciferase assays indicated that miR-139-5p interacted with the 3' untranslated region (3'-UTR) of PD1. These results showed that paeonol alleviates PD1-mediated antitumor immunity by reducing miR-139-5p expression and demonstrated a novel mechanism for melanoma immunotherapy.
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-1 (Programmed cell death 1) • MIR139 (MicroRNA 139)
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PD-1 overexpression • PD-1 expression • PD-1-L • PD-1 underexpression • miR-139-5p expression
over1year
Circ_0073228 serves as a competitive endogenous RNA to facilitate proliferation and inhibit apoptosis of hepatocellular carcinoma cells by the miR-139-5p/DNASE2 axis. (PubMed, J Gene Med)
Circ_0073228 serves as an oncogne to facilitate growth and inhibit apoptosis of HCC cells by regulating the miR-139-5p/DNASE2 axis.
Journal
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MIR139 (MicroRNA 139)
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miR-139-5p expression
over1year
Genetic and pharmacological inhibition of TUT4 and TUT7 sensitizes AML cells to BCL-2 inhibition (AACR 2023)
Inhibition of uridylation in THP-1 cells reduced proliferation, induced changes in cell cycle progression, and enhanced sensitivity to the BCL-2 inhibitor, venetoclax, alone and in combination with azacitidine. Treatment of primary AML with combination of TS-002266 and venetoclax improved activity over venetoclax alone in a number of primary AML samples. Thus, we propose that TUT4/7 and BCL-2 inactivation may be a therapeutic strategy in leukemia.
IO biomarker
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MIR139 (MicroRNA 139) • MIR494 (MicroRNA 494)
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MLL rearrangement • BCL2 expression • miR-139-5p expression
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Venclexta (venetoclax) • azacitidine
over1year
Circ_0068631 sponges miR-139-5p to promote the growth and metastasis of cutaneous squamous cell carcinoma by upregulating HOXB7. (PubMed, Skin Res Technol)
Circ_0068631 was overexpressed in CSCC tissues and cells. Circ_0068631 downregulation suppressed CSCC progression via miR-139-5p. Circ_0068631 regulated HOXB7 via sponging miR-139-5p.
Journal
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MIR139 (MicroRNA 139)
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miR-139-5p expression
almost2years
Pancreatic cancer cells upregulate LPAR4 in response to isolation stress to promote an ECM-enriched niche and support tumour initiation. (PubMed, Nat Cell Biol)
Moreover, ligation of this fibronectin-containing matrix via integrins α5β1 or αVβ3 can transfer stress tolerance to LPAR4-negative cells. Therefore, stress- or drug-induced LPAR4 enhances cell-autonomous production of a fibronectin-rich extracellular matrix, allowing cells to survive 'isolation stress' and compensate for the absence of stromal-derived factors by creating their own tumour-initiating niche.
Journal
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FN1 (Fibronectin 1) • MIR139 (MicroRNA 139)
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miR-139-5p expression
almost2years
CircNDC80 promotes glioblastoma multiforme tumorigenesis via the miR-139-5p/ECE1 pathway. (PubMed, J Transl Med)
According to our research, circNDC80 is an oncogenic factor that promotes glioblastoma through the miR-139-5p/ECE1 pathway. This implies that circNDC80 may be employed as a novel therapeutic target and a possible predictive biomarker.
Journal
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MIR139 (MicroRNA 139)
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miR-139-5p expression
almost2years
Matrine inhibits hepatocellular carcinoma cell malignancy through the circ_0013290/miR-139-5p/MMP16 pathway. (PubMed, Histol Histopathol)
Matrine inhibited HCC cell malignancy through the circ_0013290/miR-139-5p/MMP16 pathway, suggesting that Matrine is a potential therapeutic agent for HCC.
Journal
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CCND1 (Cyclin D1) • CDH2 (Cadherin 2) • MIR139 (MicroRNA 139)
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CCND1 expression • miR-139-5p expression
almost2years
Genetic and Pharmacological Inhibition of TUT4/TUT7 Sensitizes AML Cells to BCL-2 Inhibition (ASH 2022)
Inhibition of uridylation in THP-1 cells reduced proliferation, induced changes in cell cycle progression, and enhanced sensitivity to the BCL-2 inhibitor, venetoclax, alone and in combination with azacitidine. Treatment of primary AML with combination of TS-002266 and venetoclax improved activity over venetoclax alone in a number of primary AML samples. Thus, we propose that TUT4/7 and BCL-2 inactivation may be a therapeutic strategy in leukemia.
IO biomarker
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MIR139 (MicroRNA 139) • MIR494 (MicroRNA 494)
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MLL rearrangement • BCL2 expression • miR-139-5p expression
|
Venclexta (venetoclax) • azacitidine
almost2years
N6-methyladenosine-mediated SH3BP5-AS1 upregulation promotes GEM chemoresistance in pancreatic cancer by activating the Wnt signaling pathway. (PubMed, Biol Direct)
This study revealed that SH3BP5-AS1 activated Wnt signaling pathway by sponging miR-139-5p, upregulating CTBP1 expression, and contributing to the sensitivity of PC cells to GEM. SH3BP5-AS1 might be a potential target for PC therapy.
Journal
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IGF2BP1 (Insulin Like Growth Factor 2 MRNA Binding Protein 1) • CTBP1 (C-Terminal Binding Protein 1) • MIR139 (MicroRNA 139) • ALKBH5 (AlkB Homolog 5, RNA Demethylase)
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miR-139-5p expression
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gemcitabine
2years
Molecular Pathogenesis of Colorectal Cancer: Impact of Oncogenic Targets Regulated by Tumor Suppressive miR-139-3p. (PubMed, Int J Mol Sci)
The involvement of miRNA passenger strands (e.g., miR-139-3p) in CRC cells is a new concept in miRNA studies. Our tumor-suppressive miRNA-based approach helps elucidate the molecular pathogenesis of CRC.
Journal
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AKT1 (V-akt murine thymoma viral oncogene homolog 1) • HK2 (Hexokinase 2) • AGO2 (Argonaute RISC Catalytic Component 2) • MIR139 (MicroRNA 139)
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miR-139-5p expression
over2years
LncRNA RP11‑805J14.5 functions as a ceRNA to regulate CCND2 by sponging miR‑34b‑3p and miR‑139‑5p in lung adenocarcinoma. (PubMed, Oncol Rep)
Our study demonstrated that the regulation of RP11‑805J14.5 on LUAD was mediated by CCND2 whose expression was regulated by sponging miR‑34b‑3p and miR‑139‑5p. The expression of RP11‑805J14.5 was increased in LUAD, and the knockdown of RP11‑805J14.5 expression suppressed LUAD cell growth, invasion and migration by downregulating CCND2 by sponging miR‑34b‑3p and miR‑139‑5p, indicating that RP11‑805J14.5 could be a prospective target for LUAD therapy.
Journal
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CCND2 (Cyclin D2) • MIR139 (MicroRNA 139)
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miR-139-5p expression
over2years
Tumor suppressive role of microRNA-139-5p in bone marrow mesenchymal stem cells-derived extracellular vesicles in bladder cancer through regulation of the KIF3A/p21 axis. (PubMed, Cell Death Dis)
miR-139-5p in BMSCs-EVs arrested the tumorigenesis and lung metastasis of bladder cancer cells in vivo by modulation of the KIF3A/p21 axis. Altogether, BMSCs-EVs carried miR-139-5p targeted KIF3A to activate p21, thus delaying the occurrence of bladder cancer.
Journal
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MIR139 (MicroRNA 139)
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miR-139-5p expression
over2years
MicroRNA-139-5p negatively regulates NME1 expression in hepatocellular carcinoma cells. (PubMed, Adv Clin Exp Med)
The upregulation of NME1 in HCC indicates a poor prognosis. The NME1 is negatively regulated by miR-139-5p to inhibit cell proliferation.
Journal
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MIR139 (MicroRNA 139) • MIR335 (MicroRNA 335)
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miR-139-5p expression
over2years
CircRNA PTPRM Promotes Non-Small Cell Lung Cancer Progression by Modulating the miR-139-5p/SETD5 Axis. (PubMed, Technol Cancer Res Treat)
At last, we evaluated the effects of circPTPRM, SETD5, and miR-139-5p on tumor growth in vivo using BALB/c nude mice to prove the hypothesis. We thus conclude that circPTPRM promotes the progression of NSCLC by regulating the miR-139-5p/SETD5 axis.
Journal
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MIR139 (MicroRNA 139)
|
miR-139-5p expression
over2years
MiR-139-5p Inhibits the Development of Gastric Cancer through Targeting TPD52. (PubMed, J Healthc Eng)
And TPD52 upregulation weakened the antitumor effect of miR-139-5p in GC. MiR-139-5p inhibits GC cell proliferation and metastasis through downregulating TPD52.
Journal
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MIR139 (MicroRNA 139)
|
miR-139-5p expression
over2years
Exosomal circDNER enhances paclitaxel resistance and tumorigenicity of lung cancer via targeting miR-139-5p/ITGB8. (PubMed, Thorac Cancer)
The circDNER mediated miR-139-5p/ITGB8 axis suppresses lung cancer progression. Our findings suggest that circDNER might act as a potential prognostic biomarker and therapeutic target for lung cancer treatment.
Journal
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MIR139 (MicroRNA 139)
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miR-139-5p expression
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paclitaxel
over2years
miR-139-5p Was Identified as Biomarker of Different Molecular Subtypes of Breast Carcinoma. (PubMed, Front Oncol)
The expression of miR-139-5p in normal breast cells MCF-10A, human breast cancer cell line MDA-MB-231 cells, and BMSCs-derived exosomes were compared; the exosomes and MDA-MB-231 cells were co-cultured to observe their effects on the proliferation of the MDA-MB-231 cells. Human bone marrow mesenchymal stem cell-derived exosomes inhibited the growth of breast cancer cells and promoted the expression of FBN2, MEX3A, and TPD52 by transporting miR-139-5p.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • MIR139 (MicroRNA 139)
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miR-139-5p expression
over2years
Use of miRNA Sequencing to Reveal Hub miRNAs and the Effect of miR-582-3p/SMAD2 in the Progression of Hepatocellular Carcinoma. (PubMed, Front Genet)
At the same time, interference with SMAD2 can influence the effect of miR-582-3p on HepG2 cells. In conclusion, our findings confirm that miR-582-3p is an independent factor for the prognosis of hepatocellular carcinoma patients, and can regulate the progression of hepatocellular carcinoma cells by targeting SMAD2.
Journal
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MIR139 (MicroRNA 139) • MIR582 (MicroRNA 582) • SMAD2 (SMAD Family Member 2)
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miR-139-5p expression
over2years
The meta-signature guided investigation of miRNA candidates as potential biomarkers of oral cancer. (PubMed, Oral Dis)
miR-31-3p, miR-139-5p, miR-30a-5p panel was confirmed as a potential diagnostic biomarker when distinguishing oral cancer from non-cancerous tissue. miR-135b-5p, miR-18a-5p and miR-30a-5p might serve as potential biomarkers of poor survival of oral cancer patients.
Journal
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MIR21 (MicroRNA 21) • MIR135B (MicroRNA 135b) • MIR139 (MicroRNA 139) • MIR18A (MicroRNA 18a) • MIR31 (MicroRNA 31) • MIR375 (MicroRNA 375) • MIR424 (MicroRNA 424)
|
miR-135-b expression • miR-139-5p expression
over2years
MiR-139-5p/ENAH Affects Progression of Hepatocellular Carcinoma Cells. (PubMed, Biochem Genet)
Likewise, miR-139-5p was determined to perform tumor-suppressing function in vivo. MiR-139-5p hampered HCC cell processes by mediating ENAH, and miR-139-5p/ENAH is hopefully to be the possible target for HCC patients.
Journal
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MIR139 (MicroRNA 139)
|
miR-139-5p expression
over2years
GTF2E2 is a novel biomarker for recurrence after surgery and promotes progression of esophageal squamous cell carcinoma via miR-139-5p/GTF2E2/FUS axis. (PubMed, Oncogene)
Additionally, we demonstrated that GTF2E2 promotes ESCC cells progression via activation of the AKT/ERK/mTOR pathway. In conclusion, GTF2E2 may serve as a novel biomarker for recurrence after surgery and a potential therapeutic target for ESCC patients, and it promotes ESCC progression via miR-139-5p/GTF2E2/FUS axis.
Journal
|
FUS (FUS RNA Binding Protein) • AGO2 (Argonaute RISC Catalytic Component 2) • MIR139 (MicroRNA 139)
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miR-139-5p expression
over2years
MiR-139-5p Targeting CCNB1 Modulates Proliferation, Migration, Invasion and Cell Cycle in Lung Adenocarcinoma. (PubMed, Mol Biotechnol)
CCNB1 overexpression fostered progression of LUAD cells. Mechanistically, miR-139-5p might negatively regulate CCNB1 in LUAD, thereby suppressing cell proliferation, migration, invasion and cell cycle.
Journal
|
MIR139 (MicroRNA 139) • CCNB1 (Cyclin B1)
|
miR-139-5p expression
almost3years
MicroRNA-139-5p Suppresses Cell Malignant Behaviors in Breast Cancer through Targeting MEX3A. (PubMed, Comput Math Methods Med)
MicroRNA-139-5p inhibited the development of BC by targeting MEX3A. MicroRNA-139-5p/MEX3A may be a target for BC therapy.
Journal
|
MIR139 (MicroRNA 139)
|
miR-139-5p expression
almost3years
Systematic analysis of the role of SLC52A2 in multiple human cancers. (PubMed, Cancer Cell Int)
In conclusion, we have systematically described for the first time that SLC52A2 is closely associated with a variety of tumors, especially hepatocellular carcinoma.
Journal • Tumor Mutational Burden
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TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • MIR139 (MicroRNA 139)
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miR-139-5p expression
3years
miR-139-5p sponged by LncRNA NEAT1 regulates liver fibrosis via targeting β-catenin/SOX9/TGF-β1 pathway. (PubMed, Cell Death Discov)
LncRNA NEAT1 exacerbated liver fibrosis by suppressing the expression of miR-139-5p. Collectively, our study suggested that miR-139-5p sponged by lncRNA NEAT1 regulated liver fibrosis via targeting β-catenin/SOX9/TGF-β1 Pathway.
Journal
|
SOX9 (SRY-Box Transcription Factor 9) • TGFB1 (Transforming Growth Factor Beta 1) • MIR139 (MicroRNA 139)
|
miR-139-5p expression
3years
Roles of the miR-139-5p/CCT5 axis in hepatocellular carcinoma: a bioinformatic analysis. (PubMed, Int J Med Sci)
MiR-139-5p suppresses HCC tumor aggression and conversely correlated with CCT5. The miR-139-5p/CCT5 axis might perform crucial functions in the development of HCC.
Journal
|
AFP (Alpha-fetoprotein) • MIR139 (MicroRNA 139)
|
miR-139-5p expression
3years
Exosomal transfer of tumor-associated macrophage-derived hsa_circ_0001610 reduces radiosensitivity in endometrial cancer. (PubMed, Cell Death Dis)
In vivo, the promotion effect of EXOs on xenograft tumor growth in nude mice treated with irradiation was further reinforced after hsa_circ_0001610 overexpression. In conclusion, TAM-derived exosomes transferred hsa_circ_0001610 to EC cells, and the overexpressed hsa_circ_0001610 in EC cells released cyclin B1 expression through adsorbing miR-139-5p, thereby weakening the radiosensitivity of EC cells.
Journal
|
MIR139 (MicroRNA 139) • CCNB1 (Cyclin B1)
|
miR-139-5p expression
over3years
MicroRNA-139-5p Regulates Fibrotic Potentials via Modulation of Collagen Type 1 and Phosphorylated p38 MAPK in Uterine Leiomyoma. (PubMed, Yonsei Med J)
Expression of miR-139-5p is downregulated in leiomyoma cells and modulation of miR-139-5p may be involved inthe pathogenesis of leiomyomas through the regulation of collagen type 1 and phosphorylated p38 MAPK. Therefore, miR-139-5p is a potential therapeutic target for leiomyoma.
Journal
|
MIR139 (MicroRNA 139)
|
miR-139-5p expression