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Related Concept Videos

MicroRNAs01:22

MicroRNAs

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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...
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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...
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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
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miR-7 Reduces Breast Cancer Stem Cell Metastasis via Inhibiting RELA to Decrease ESAM Expression.

Miao Li1, Meng Pan1,2, Jing Wang3

  • 1Department of Pathogenic Biology and Immunology, School of Medicine, Southeast University, Nanjing 210009, China.

Molecular Therapy Oncolytics
|July 9, 2020
PubMed
Summary
This summary is machine-generated.

MicroRNA-7 (miR-7) effectively inhibits breast cancer stem cell metastasis by targeting the endothelial cell-selective adhesion molecule (ESAM). This discovery suggests ESAM as a potential therapeutic target for reducing breast cancer spread.

Keywords:
breast cancerbreast cancer stem cellsendothelial cell-selective adhesion moleculeendothelial cell-selective adhesion molecule(ESAM)metastasismiR-7

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Breast cancer stem cells (BCSCs) are crucial drivers of metastasis.
  • The precise mechanisms by which miR-7 inhibits BCSCs metastasis are not fully understood.
  • Endothelial cell-selective adhesion molecule (ESAM) is implicated in cancer progression.

Purpose of the Study:

  • To investigate the inhibitory effect of miR-7 on breast cancer stem cell (BCSC) metastasis.
  • To elucidate the underlying molecular mechanisms of miR-7's action.
  • To evaluate ESAM as a potential therapeutic target in breast cancer.

Main Methods:

  • Protein array analysis of BCSC-driven tumors.
  • Dual-luciferase reporter assays and chromatin immunoprecipitation-PCR (ChIP-PCR) to validate molecular targets.
  • In vivo studies using mouse models of BCSC-driven xenografts.
  • Assessment of miR-7 overexpression effects on metastasis, tumor growth, and specific protein markers.

Main Results:

  • miR-7 overexpression significantly reduced BCSCs metastasis in vivo.
  • miR-7 directly targets RELA, inhibiting downstream ESAM expression in MDA-MB-231 cells.
  • ESAM was highly expressed in breast cancer tissues and xenografts.
  • Lentivirus-mediated miR-7 delivery decreased RELA, CD44, and ESAM levels, while increasing E-cadherin and decreasing vimentin in xenografts.
  • Tumor growth and lung metastasis were reduced in mice treated with Lenti-miR-7.

Conclusions:

  • miR-7 inhibits breast cancer stem cell metastasis by suppressing ESAM expression through the RELA pathway.
  • ESAM represents a promising therapeutic target for inhibiting breast cancer progression and metastasis.
  • Understanding the miR-7/RELA/ESAM axis provides new insights into breast cancer stem cell biology and therapeutic strategies.