ArticleCancer biology & therapy2020
STAT4-mediated down-regulation of miR-3619-5p facilitates stomach adenocarcinoma by modulating TBC1D10B.
Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Deciphering the role of LOC124905135-related non-coding RNA cluster in human cancers: A comprehensive review.Heliyon · 2024Review
- TBC1D10B promotes tumor progression in colon cancer via PAK4‑mediated promotion of the PI3K/AKT/mTOR pathway.Apoptosis : an international journal on programmed cell death · 2024Article
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- Transcription factor E2F3 activates CDC25B to regulate DNA damage and promote mitoxantrone resistance in stomach adenocarcinoma.Molecular biology reports · 2024Article
- Identification of memory B-cell-associated miRNA signature to establish a prognostic model in gastric adenocarcinoma.Journal of translational medicine · 2023Article
- Increased expression of TBC1D10B as a potential prognostic and immunotherapy relevant biomarker in liver hepatocellular carcinoma.Scientific reports · 2023Article
- M2 macrophage facilitated angiogenesis in cutaneous squamous cell carcinoma via circ_TNFRSF21/miR-3619-5p/ROCK axis.The Kaohsiung journal of medical sciences · 2022Article
- NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1.Cancer cell international · 2022Article
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
backgroundMicroRNAs (miRNAs) as the subtype of non-coding RNAs are revealed to be crucial players in cellular activities. It has been reported that miR-3619-5p functions as a tumor inhibitor in several cancers. However, the connection between miR-3619-5p and stomach adenocarcinoma (STAD) remains to be discovered. AIM OF THE STUDY: The purpose of the study is to figure out the role and molecular regulation mechanism of miR-3619-5p in STAD.
methodsThe expression of miR-3619-5p was evaluated via qRT-PCR analysis. Gain-of-function experiments demonstrated the effects of miR-3619-5p on cellular functions. The upper-stream transcription factor STAT4 and downstream target gene TBC1D10B of miR-3619-5p were identified by bioinformatic analysis. The binding and interaction between the indicated molecules were verified by RNA pull-down and luciferase reporter assays.
resultsThe expression of miR-3619-5p was prominently down-regulated in STAD cells and tissues. MiR-3619-5p suppresses cell proliferation, migration, invasion and tumor growth in STAD. Further, STAT4 bound with miR-3619-5p promoter and inhibited its transcription. MiR-3619-5p was also recognized to modulate STAD progression through the regulation of downstream target gene TBC1D10B.
conclusionSTAT4-mediated miR-3619-5p controls STAD carcinogenesis and progression through modulating TBC1D10B expression, which may provide a novel insight for researching the STAD-related molecular mechanism.
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