ArticleCancer cell international2018
MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 52 citations in OpenAlex.
- Hepatoma-derived growth factor and non-coding RNA network in ovarian cancer patients.Biochemistry and biophysics reports · 2025Article
- The Circular RNA Circ_0043947 Promoted Gastric Cancer Progression by Sponging miR-384 to Regulate CREB1 Expression.Gut and liver · 2024Article
- MicroRNA-384 radiosensitizes human non-small cell lung cancer by impairing DNA damage response and repair signaling, which is inhibited by NF-κB.Cancer biology & medicine · 2024Article
- Review
- In silico analysis to identify miR-1271-5p/PLCB4 (phospholipase C Beta 4) axis mediated oxaliplatin resistance in metastatic colorectal cancer.Scientific reports · 2023Article
- LncRNA PVT1 regulates biological function of osteoarthritis cells by regulating miR-497/AKT3 axis.Medicine · 2022Article
- Circular RNA PVT1 promotes progression of thyroid cancer by competitively binding miR-384.Experimental and therapeutic medicine · 2022Article
- miR-3614-3p suppresses cell aggressiveness of human breast cancer by targetingTranslational cancer research · 2022Article
- Hypomethylation-driven AKT Serine/Threonine Kinase 3 promotes testicular germ cell tumors proliferation and negatively correlates to immune infiltration.Bioengineered · 2021Article
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- Comprehensive analysis of lncRNA-associated ceRNA network reveals the novel potential of lncRNA, miRNA and mRNA biomarkers in human rectosigmoid junction cancer.Oncology letters · 2021Article
- RHPN1-AS1 promotes cell proliferation and migration via miR-665/Akt3 in ovarian cancer.Cancer gene therapy · 2021Article
- Syntaxin 2 promotes colorectal cancer growth by increasing the secretion of exosomes.Journal of Cancer · 2021Article
- Inhibition of miR-185-3p Confers Erlotinib Resistance Through Upregulation of PFKL/MET in Lung Cancers.Frontiers in cell and developmental biology · 2021Article
- Silencing long non-coding RNA CASC9 inhibits colorectal cancer cell proliferation by acting as a competing endogenous RNA of miR-576-5p to regulate AKT3.Cell death discovery · 2020Article
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- Identification of microRNAs and their Endonucleolytic Cleavaged target mRNAs in colorectal cancer.BMC cancer · 2020Article
- Article
- Down-regulation of lncRNA UCA1 enhances radiosensitivity in prostate cancer by suppressing EIF4G1 expression via sponging miR-331-3p.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGrowing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown.
methodsThe expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman's correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC.
resultsMiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3.
conclusionOur study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.
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