Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Oncol Rep. 2010 Jun;23(6):1625-33.

Expression of microRNAs in squamous cell carcinoma of human head and neck and the esophagus: miR-205 and miR-21 are specific markers for HNSCC and ESCC.

Author information

  • 1Division of Tumor Pathology, Department of Pathological Sciences, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.

Abstract

MicroRNAs (miRNAs) are non-coding small RNAs that regulate cell proliferation and functions by interfering with the translation of target mRNAs. Altered expression of miRNA is known to induce various human malignancies. We examined the expression of miRNAs in squamous cell carcinoma of human head and neck (HNSCC) and esophagus (ESCC), compared to that in normal squamous epithelia as well as malignancies of other organs. Microarray analysis showed up-regulation of miR-21, miR-16 and miR-30a-5p in HNSCC and ESCC cell lines compared to normal squamous epithelial cell lines, and consistent high expression of miR-205 and let-7a in both normal and malignant squamous epithelial cell lines. Validation study using real-time quantitative RT-PCR in formalin-fixed paraffin-embedded cancer tissues and paired normal epithelia obtained by Laser-captured microdissection revealed that miR-205 showed highest expression in both malignant and benign squamous epithelia, although it was less expressed in cell lines and tissues other than squamous epithelia. MiR-21, which is an oncogenic miRNA in various malignancies, was also up-regulated in HNSCC and ESCC compared to paired normal squamous epithelia. These results suggest that miR-205 might be a specific marker miRNA of both normal and malignant squamous epithelia, while miR-21 might be a putative oncogenic miRNA in HNSCC and ESCC.

PMID:
20428818
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Spandidos Publications
    Loading ...
    Write to the Help Desk