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Telomerase activity in head and neck tumors after introduction of wild‐type p53, p21, p16, and E2F‐1 genes by means of recombinant adenovirus
Author(s) -
Henderson Ying C.,
Breau Randall L.,
Liu TaJen,
Clayman Gary L.
Publication year - 2000
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/1097-0347(200007)22:4<347::aid-hed6>3.0.co;2-j
Subject(s) - telomerase , telomerase reverse transcriptase , cell culture , cancer research , biology , telomere , e2f , cell growth , microbiology and biotechnology , cell cycle , cell , gene , genetics
Background Telomerase (reverse transcriptase) has been shown to play a role in the process of cellular immortalization. Methods Telomerase activity was determined in 11 head and neck squamous cell carcinoma (SCCHN) cell lines. The effects of wild‐type p16, p21, E2F‐1, and p53 genes on telomerase activity were examined by introducing the wild‐type genes into two SCCHN cell lines by means of a recombinant adenovirus. Results We found elevated telomerase activity in 10 of the 11 SCCHN cell lines tested. When we infected Tu‐138 and Tu‐167 cell lines with wild‐type p16, p21, E2F‐1, and p53 genes, we found that p16 had little effect on telomerase activity. Both E2F‐1 and p53 were known to induce apoptosis in SCCHN cell lines. Significantly reduced telomerase activity by p53 in both cell lines and E2F‐1 in Tu‐167 cells was in agreement with suppression of cell growth. Overexpression of p21 also exhibited reduction in telomerase activity. Conclusions We conclude from this study that overexpression of E2F‐1 and p53 can reverse telomerase activity in SCCHN cell lines and that telomerase activity may be involved in cancer cell immortalization. © 2000 John Wiley & Sons, Inc. Head Neck 22: 347–354, 2000.