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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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KRAS Cold Turkey: Using microRNAs to target KRAS-addicted cancer.

Matthew F Jones1, Toshifumi Hara1,2, Ashish Lal1

  • 1Regulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

RNA & Disease (Houston, Tex.)
|January 26, 2018
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MicroRNAs (miRNAs) can selectively target KRAS-mutant colon cancer cells. MiR-126 induces synthetic lethality in these cells by down-regulating key growth pathways, offering a novel therapeutic strategy.

Keywords:
KRASRAScolorectal cancermiR-216miRNAsynthetic lethality

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Human cancers are driven by genetic mutations activating pro-growth pathways.
  • KRAS mutations are common, drug-resistant drivers in colon cancer, with tumors exhibiting addiction to signaling proteins outside the KRAS pathway.
  • MicroRNAs (miRNAs) are key gene regulators frequently dysregulated in cancer.

Purpose of the Study:

  • To identify miRNAs that selectively inhibit the survival of KRAS-mutant cancer cells.
  • To explore novel therapeutic strategies targeting KRAS-mutant cancers.

Main Methods:

  • Functional miRNA screening to identify tumor-suppressive miRNAs in KRAS-mutant cells.
  • Investigating the mechanism of action for identified miRNAs, including target gene identification.

Main Results:

  • MiR-126 was identified as a miRNA selectively inhibiting KRAS-mutant cell survival.
  • MiR-126 induced synthetic lethality in KRAS-mutant cells.
  • Down-regulation of the polo-like kinase signaling network and other essential genes for KRAS-mutant tumor growth was observed.

Conclusions:

  • MiRNAs represent a promising therapeutic avenue for targeting KRAS-mutant cancers.
  • MiR-126 demonstrates potential as a selective agent against KRAS-driven colon tumors.
  • Targeting aberrant cell signaling through miRNAs offers a new strategy for cancer treatment.