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Induction and Testing of Hypoxia in Cell Culture
07:01

Induction and Testing of Hypoxia in Cell Culture

Published on: August 12, 2011

aHIF: a natural antisense transcript overexpressed in human renal cancer and during hypoxia

C A Thrash-Bingham1, K D Tartof

  • 1Fox Chase Cancer Center, Philadelphia, PA, USA.

Journal of the National Cancer Institute
|January 29, 1999
PubMed
Abstract

Insights

A novel natural antisense transcript, aHIF, is overexpressed in nonpapillary renal carcinoma, unlike papillary types. This discovery marks the first antisense transcript exclusively linked to a specific human cancer.

Area of Science:

  • Molecular biology
  • Cancer research
  • Genetics

Background:

  • Nonpapillary renal carcinoma is a distinct subtype of kidney cancer.
  • Hypoxia-inducible factor alpha (HIF1alpha) plays crucial roles in cellular responses to oxygen levels.
  • A natural antisense transcript, aHIF, complementary to HIF1alpha mRNA, was identified.

Purpose of the Study:

  • To characterize the natural antisense transcript aHIF.
  • To investigate the expression of aHIF in different types of renal carcinoma.
  • To understand the relationship between aHIF, HIF1alpha, and cellular conditions.

Main Methods:

  • Differential display
  • Reverse transcription-polymerase chain reaction (RT-PCR)
  • Ribonuclease protection assay
  • DNA sequencing

Main Results:

  • aHIF is a natural antisense transcript derived from HIF1alpha gene sequences.
  • aHIF is specifically overexpressed in nonpapillary clear-cell renal carcinomas but not in papillary renal carcinomas.
  • aHIF is overexpressed in nonpapillary renal carcinoma cells under both normoxic and hypoxic conditions.
  • Hypoxia induces aHIF in lymphocytes, with a concurrent decrease in HIF1alpha mRNA.

Conclusions:

  • This study reports the first natural antisense transcript exclusively overexpressed in a specific human malignancy.
  • aHIF represents a potential diagnostic marker for nonpapillary renal carcinoma.
  • The findings provide new insights into the molecular mechanisms of nonpapillary renal carcinoma development.

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