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.

Genes & Genomics
|April 28, 2021
PubMed
Abstract

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.

Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.3K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
22.8K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.0K