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Differential expression of nuclear retinoid receptors in normal, premalignant, and malignant head and neck tissues

X C Xu1, J Y Ro, J S Lee

  • 1Department of Tumor Biology, University of Texas, M.D. Anderson Cancer Center, Houston 77030.

Cancer Research
|July 1, 1994
PubMed

Insights

Decreased expression of the retinoic acid receptor-beta (RAR-beta) may be linked to head and neck squamous cell carcinoma (HNSCC) development. This study investigated retinoid receptor mRNA in normal and cancerous tissues.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Retinoids are known to reverse premalignant lesions and prevent new cancers in upper aerodigestive tract cancer patients.
  • Nuclear retinoid receptors, including retinoic acid receptors (RARs) and retinoid X receptors (RXRs), mediate retinoid actions.
  • Alterations in RAR and RXR expression are hypothesized to contribute to cancer development.

Purpose of the Study:

  • To investigate the relationship between the expression of RAR and RXR mRNAs and the development of head and neck squamous cell carcinoma (HNSCC).

Main Methods:

  • In situ hybridization was performed on histological sections from normal volunteers and HNSCC patients.
  • Digoxigenin-labeled antisense riboprobes were used to detect mRNAs for RAR-alpha, RAR-beta, RAR-gamma, RXR-alpha, and RXR-beta.
  • Expression levels were analyzed in normal, hyperplastic, dysplastic, and malignant tissues.

Main Results:

  • All 5 receptors (RAR-alpha, RAR-beta, RAR-gamma, RXR-alpha, RXR-beta) were expressed in normal tissues.
  • RAR-gamma, RXR-alpha, and RXR-beta mRNA levels were similar across normal, hyperplastic, dysplastic, and malignant tissues.
  • RAR-alpha mRNA expression decreased slightly in HNSCC compared to normal tissues.
  • RAR-beta mRNA expression showed a significant decrease in HNSCC (35%) and dysplastic lesions (56%) compared to adjacent normal tissues (approx. 70%).

Conclusions:

  • The decreased expression of RAR-beta mRNA is significantly associated with the development of head and neck squamous cell carcinoma.
  • These findings suggest a potential role for RAR-beta downregulation in HNSCC pathogenesis.

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