ArticleYonsei medical journal2022
MiR-103a-3p Contributes to the Progression of Colorectal Cancer by Regulating GREM2 Expression.
Article in Yonsei medical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
- Regulation of ferroptosis in colorectal cancer through therapeutic modulation and miRNA targeting.Biochemistry and biophysics reports · 2026Article
- Targeting miR-103a-3p/IGFBP5 axis: a potential therapeutic strategy for gastric cancer progression.Discover oncology · 2025Article
- Targeting Regulatory Noncoding RNAs in Human Cancer: The State of the Art in Clinical Trials.Pharmaceutics · 2025Review
- Crosstalk between non-coding RNAs and programmed cell death in colorectal cancer: implications for targeted therapy.Epigenetics & chromatin · 2025Review
- Exploratory research on therapeutic agents combined with early diagnostic biomarkers for colorectal cancer.Frontiers in pharmacology · 2025Article
- Gremlin-2 is a novel tumor suppressor that negatively regulates ID1 in breast cancer.Breast cancer research : BCR · 2024Article
- Non-Coding RNAs of Mitochondrial Origin: Roles in Cell Division and Implications in Cancer.International journal of molecular sciences · 2024Review
- Signaling pathways in colorectal cancer implications for the target therapies.Molecular biomedicine · 2024Review
- A Comprehensive Understanding of Post-Translational Modification of Sox2 via Acetylation andCancers · 2024Article
- CYTOR Promotes Proliferation of Lung Cancer Cell by Targeting miR-103a-3p to Upregulate HMGB1.Molecular biotechnology · 2023Article
- Significant role of circRNA BBS9 in chronic obstructive pulmonary disease via miRNA-103a-3p/BCL2L13.BMC pulmonary medicine · 2023Article
- Clinical significance of LINC00893 and miR-103a-3p in type 2 diabetes mellitus patients with coronary heart disease.Diabetes & vascular disease researchArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
purposeOur research aimed to investigate the influence of miR-103a-3p on the growth and apoptosis of colorectal cancer (CRC) cells. MATERIALS AND
methodsBioinformatics was employed to analyze differentially expressed microRNAs and predict target genes. qRT-PCR was applied to detect the expression of miR-103a-3p in CRC and normal cells. HCT116 and Caco-2 were chosen, and miR-103a-3p mimics, miR-103a-3p inhibitor, as well as specific siRNAs targeting GREM2, were constructed. We subsequently evaluated alternations in cell proliferation, cell cycle and cell cycle regulators, apoptosis, and related proteins (Bcl-2 and Bax) by CCK-8 testing, Western blotting, luciferase reporter, colony formation, and Annexin V-FITC/PI. Possible binding sites for miR-103a-3p on the 3'UTR of GREM2 were checked with luciferase assay, and the impact of GREM2 on miR-103a-3p activity was also validated with above biological function testing. Additionally, the effect of miR-103a-3p knockdown in CRC cells and the molecular mechanism of miR-103a-3p targeting GREM2 were also studied.
resultsBioinformatics analysis revealed that miR-103a-3p expression increased remarkably in CRC, and targeted regulatory correlation existed between miR-103a-3p and GREM2. MiR-103a-3p inhibitor significantly impeded proliferative capacity and caused cell cycle arrest, as well as apoptosis, in HCT116 and Caco-2 cells. Consistent with this finding, overexpression of GREM2 showed similar effects to miR-103a-3p inhibition. Moreover, we demonstrated that miR-103a-3p connected target GREM2 and GREM2 knockdown reversed the effects of miR-103a-3p inhibitor on HCT116 and Caco-2 cell proliferation, cell cycle, and apoptosis. Further study showed that miR-103a-3p targeting GREM2 appeared to affect CRC progression via the transforming growth factor-β pathway.
conclusionMiR-103a-3p could augment CRC progression by targeting GREM2 and that miR-103a-3p/GREM2 could be potential novel targets for CRC therapy.
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