ArticleExperimental and therapeutic medicine2018
MicroRNA-222 regulates the viability of fibroblasts in hypertrophic scars via matrix metalloproteinase 1.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Early intervention of carbon dioxide fractional laser in hypertrophic scar through TGFβ-1/ Smad3 signaling pathway.Lasers in medical science · 2024Article
- Preparation of tanshinone IIChinese herbal medicines · 2023Article
- miR-623 Targets Metalloproteinase-1 and Attenuates Extravasation of Brain Metastatic Triple-Negative Breast Cancer Cells.Breast cancer (Dove Medical Press) · 2022Article
- Regulation of breast cancer metastasis signaling by miRNAs.Cancer metastasis reviews · 2020Review
- Silencing miR-202-3p increases MMP-1 and promotes a brain invasive phenotype in metastatic breast cancer cells.PloS one · 2020Article
- MicroRNA-222 reprogrammed cancer-associated fibroblasts enhance growth and metastasis of breast cancer.British journal of cancer · 2019Article
- MicroRNA hsa-miR-623 directly suppresses MMP1 and attenuates IL-8-induced metastasis in pancreatic cancer.International journal of oncology · 2019Article
- Article
- Inhibition of miR-9 attenuates fibroblast proliferation in human hyperplastic scar by regulating TGF-β1.American journal of translational research · 2019Article
- Non-Coding RNAs in Breast Cancer: Intracellular and Intercellular Communication.Non-coding RNA · 2018Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to determine the expression of microRNA (miR)-222 in hypertrophic scar (HS) tissues, and investigate the regulatory mechanism of miR-222 in HS. A total of 36 patients diagnosed with HS between August 2013 and May 2016 were included in the present study. HS tissues and HS-adjacent tissues were collected from patients. Primary fibroblasts were obtained from HS tissue. Reverse transcription-quantitative polymerase chain reaction was used to measure mRNA levels of matrix metalloproteinase 1 (MMP1) and miR-222. Western blotting was conducted to determine MMP1 expression and an MTT assay was performed to measure the viability of fibroblasts. A dual luciferase reporter assay was used to identify the binding of miR-222 to MMP1 mRNA. It was demonstrated that MMP1 serves a role in HS at the transcription level and that increased MMP1 expression inhibited the viability of fibroblasts. miR-222 serves a regulatory role in HS by targeting its target gene MMP1 and regulates the expression of MMP1 by binding to its 3'-untranslated region. The decreased expression of miR-222 suppresses the viability of fibroblasts by regulating MMP1 expression. The present study demonstrated that the downregulation of MMP1 in HS tissues is associated with the upregulation of miR-222 expression. miR-222 may therefore regulate the viability of fibroblasts in HS and the expression of related proteins via MMP1.
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