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Related Concept Videos

MicroRNAs01:22

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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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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells.
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Related Experiment Video

Updated: Mar 25, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
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A microRNA-mediated decrease in eukaryotic initiation factor 2α promotes cell survival during PS-341 treatment.

Lili Jiang1, Dan Zang1, Songgang Yi1

  • 1State Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Department of Pathophysiology, Guangzhou Medical University, Guangdong 510182, People's Republic of China.

Scientific Reports
|February 23, 2016
PubMed
Summary
This summary is machine-generated.

Certain microRNAs (miRs), including miR-30b-5p and miR-30c-5p, promote cancer cell survival under endoplasmic reticulum (ER) stress by targeting eIF2α and inhibiting apoptosis. Inhibiting these miRs enhances cancer cell sensitivity to proteasome inhibitors.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • MicroRNAs (miRs) are key regulators in carcinogenesis.
  • Cancer cells exploit the adaptive endoplasmic reticulum (ER) stress response for survival.
  • Proteasome inhibitors are used in cancer therapy but cancer cells develop resistance.

Purpose of the Study:

  • To investigate the role of specific miRs in cancer cell adaptation to ER stress.
  • To identify novel mechanisms by which cancer cells survive ER stress.
  • To explore potential therapeutic targets for overcoming resistance to proteasome inhibitors.

Main Methods:

  • Treatment of HepG2 and MDA-MB-453 cells with proteasome inhibitor PS-341.
  • Quantification of miR expression levels.
  • Assessment of cell proliferation and apoptosis.
  • Validation of miR targets using molecular assays.
  • Analysis of the p-eIF2α/ATF4/CHOP pathway.

Main Results:

  • PS-341 treatment upregulated miR-30b-5p and miR-30c-5p.
  • These miRs promoted cell proliferation and inhibited apoptosis.
  • eIF2α was identified as a direct target of miR-30b-5p and miR-30c-5p.
  • Upregulation of these miRs suppressed the pro-apoptotic p-eIF2α/ATF4/CHOP pathway during ER stress.
  • Inhibition of miR-30b-5p or miR-30c-5p sensitized cells to PS-341 cytotoxicity.

Conclusions:

  • A novel miR-based mechanism involving miR-30b-5p and miR-30c-5p promotes cancer cell survival during ER stress.
  • These miRs maintain proteostasis by targeting eIF2α and inhibiting the pro-apoptotic pathway.
  • miR-30b-5p and miR-30c-5p represent potential therapeutic targets for anti-cancer strategies.