ArticleGenes & genomics2022
Research on the effect of interfering with miRNA-155 on triple-negative breast cancer cells.
Article in Genes & genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Exercise-associated microRNA programs as candidate modulators and biomarkers in glioblastoma: a narrative review.Discover oncology · 2026Review
- Pyroptosis in cancer therapy: a double-edged sword for immune activation and tumor progression.Molecular cancer · 2025Review
- Regulatory Effects ofFood science & nutrition · 2025Article
- Non-coding RNAs, a double-edged sword in breast cancer prognosis.Cancer cell international · 2025Review
- A potential immunotherapy target for breast cancer: parenchymal and immune-stromal expression of the NLRP3 inflammasome pathway.BMC cancer · 2023Article
- A Smart Nano-Theranostic Platform Based on Dual-microRNAs Guided Self-Feedback Tetrahedral Entropy-Driven DNA Circuit.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer.Discover oncology · 2023Review
- Regulation of Inflammasome by microRNAs in Triple-Negative Breast Cancer: New Opportunities for Therapy.International journal of molecular sciences · 2023Review
- Identification of Five Cytotoxicity-Related Genes Involved in the Progression of Triple-Negative Breast Cancer.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple negative breast cancer (TNBC) is a poor prognosis breast cancer with the highest mutation rate and limited treatment options. MiR-155 is highly expressed in TNBC, but its role and potential mechanism in TNBC remain to be elucidated.
objectiveThe aim of this study is to examine the effect of interfering with miRNA-155 on the inflammatory pathway of NLRP 3 in TNBC (MDA-MB-231).
methodsMiRNA-155-specific interference (Si-miR-155) on MDA-MB-231 cell was manifested by transfection of miRNA-155 inhibitor. Meanwhile, blank control (Blank) and negative control (NC) were set. Cell growth and proliferation rate were detected by MTT; apoptosis rate were detected by flow cytometry; colony forming test was used to detected cell viability; cell migration ability was detected by Wound healing assay; TNF-α, IL-18, IL-6 and IL-1β levels were detected by ELISA. The mRNA of miRNA-155, NLRP3, ASC, caspase-1 and Ki67 were detected by qRT-PCR. The expression levels of NLRP3, caspase-1, ASC and Ki67 were detected by Western blotting.
resultsThe proliferation rate of Si-miRNA-155 group decreased, while the apoptosis rate increased significantly. After interfering with miRNA-155, the number of cancer cell colonies and the migration ability was decreased, and the secretion levels of IL-18, TNF-α, IL-6 and IL-1β were also inhibited. Moreover the mRNA and protein expression of NLRP3, caspase-1, ASC and Ki67 were significantly suppressed.
conclusionsInterference with miRNA-155 can inhibit the NLRP3 pathway of MDA-MB-231 cells, as well as the proliferation, migration and inflammatory factor secretion of MDA-MB-231 cell, and can accelerate its apoptosis.
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