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Updated: Nov 7, 2025

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
Research on the effect of interfering with miRNA-155 on triple-negative breast cancer cells
Yangying Hu1, Deqi Wu1, Xiangjun Feng2
1Department of Thyroid and Breast Diagnosis and Treatment Center, Shulan (Hangzhou) Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College, Hangzhou, 310000, China.
Background:
Triple 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.
Objective:
The 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).
Methods:
MiRNA-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.
Results:
The 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.
Conclusions:
Interference 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.
Insights
Interfering with microRNA-155 (miR-155) inhibits triple-negative breast cancer (TNBC) cell proliferation and inflammation. This study demonstrates that targeting miR-155 can accelerate apoptosis and reduce migration in TNBC cells.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Triple-negative breast cancer (TNBC) presents a poor prognosis due to its high mutation rate and limited therapeutic strategies.
- MicroRNA-155 (miR-155) is upregulated in TNBC, but its precise role and underlying mechanisms require further investigation.
Purpose of the Study:
- To investigate the impact of inhibiting miR-155 on the NLRP3 inflammasome pathway in MDA-MB-231 TNBC cells.
- To elucidate the effects of miR-155 interference on TNBC cell proliferation, apoptosis, migration, and inflammatory cytokine secretion.
Main Methods:
- MDA-MB-231 cells were treated with a miRNA-155 inhibitor (Si-miR-155), with blank and negative controls.
- Cell proliferation, apoptosis, viability, and migration were assessed using MTT, flow cytometry, colony formation assays, and wound healing assays, respectively.
- Inflammatory markers (TNF-α, IL-18, IL-6, IL-1β) and key pathway components (miRNA-155, NLRP3, ASC, caspase-1, Ki67) were quantified via ELISA, qRT-PCR, and Western blotting.
Main Results:
- Si-miR-155 treatment significantly reduced proliferation and colony formation while increasing apoptosis in MDA-MB-231 cells.
- Inhibition of miR-155 decreased cell migration and suppressed the secretion of inflammatory cytokines (IL-18, TNF-α, IL-6, IL-1β).
- The mRNA and protein expression of NLRP3, ASC, caspase-1, and Ki67 were significantly downregulated following miR-155 interference.
Conclusions:
- Inhibiting miR-155 effectively suppresses the NLRP3 inflammasome pathway in TNBC cells.
- Targeting miR-155 demonstrates potential in reducing TNBC cell proliferation, migration, and inflammatory responses, while promoting apoptosis.
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