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Malignant transformation of colonic epithelial cells by a colon-derived long noncoding RNA

Jeffrey L Franklin1, Carl R Rankin, Shawn Levy

  • 1Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, United States; Department of Medicine, Vanderbilt University, Nashville, TN 37232, United States; Department of Veterans Affairs Medical Center, Nashville, TN 37232, United States.

Biochemical and Biophysical Research Communications
|September 19, 2013
PubMed

Insights

Long non-coding RNAs (lncRNAs) are newly explored in colon health. A specific lncRNA, ncNRFR, drives malignant transformation in colon cells by inhibiting tumor suppressor let-7.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • While protein-coding genes and microRNAs (miRNAs) roles in colonic epithelia are known, long non-coding RNAs (lncRNAs) involvement in colonic homeostasis remains largely uncharacterized.
  • Understanding lncRNA function is crucial for comprehending colonic epithelial cell regulation and disease development.

Purpose of the Study:

  • To investigate the role of lncRNAs in colonic homeostasis.
  • To identify specific lncRNAs expressed in different compartments of the adult mouse colonic crypt.
  • To characterize the function of a novel lncRNA, ncNRFR, in colon cell transformation.

Main Methods:

  • Gene expression profiling of microdissected adult mouse colonic crypts, distinguishing between differentiated tops and proliferative bottoms.
  • Stable overexpression of the identified lncRNA, ncNRFR, in immortalized mouse colonocytes.
  • Assessing malignant transformation through soft agar growth assays and in vivo tumor formation in nude mice.
  • Investigating the interaction of ncNRFR with the tumor suppressor let-7.

Main Results:

  • Several lncRNAs were found to be more highly expressed in the proliferative crypt bottom compartment.
  • A novel lncRNA, non-coding Nras functional RNA (ncNRFR), was identified within the Nras locus.
  • Overexpression of ncNRFR induced malignant transformation of mouse colonocytes, evidenced by anchorage-independent growth and invasive tumor formation.
  • ncNRFR was shown to inhibit the function of the tumor suppressor let-7.

Conclusions:

  • Precise regulation of ncNRFR is essential for normal cell growth and proliferation in the colonic crypt.
  • Misregulation of ncNRFR can lead to neoplastic transformation of colonic epithelial cells.
  • ncNRFR represents a potential therapeutic target for colon cancer.
Keywords:
BrdUColonColorectal cancerGSEAISHIntestineNon-coding RNAPCCPCRProgenitor cellsUTRsYAMCYoung adult mouse colonaRNAamplified RNAbromodeoxyuridinedays postcoitusdpcgene set enrichment analysisin situ hybridizationlet-7lncRNAslong non-coding RNAsncNRFRnon-coding Nras functional RNApolymerase chain reactionprogenitor cell compartmentsiRNAsmall interfering RNAsuntranslated regions

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