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通过重组腺病毒导入野生型p53、p21、p16和E2F-1基因后头颈部肿瘤中的端粒酶活性

Telomerase activity in head and neck tumors after introduction of wild-type p53, p21, p16, and E2F-1 genes by means of recombinant adenovirus.

作者信息

Henderson Y C, Breau R L, Liu T J, Clayman G L

机构信息

Department of Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.

出版信息

Head Neck. 2000 Jul;22(4):347-54. doi: 10.1002/1097-0347(200007)22:4<347::aid-hed6>3.0.co;2-j.

DOI:10.1002/1097-0347(200007)22:4<347::aid-hed6>3.0.co;2-j
PMID:10862017
Abstract

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.

摘要

背景

端粒酶(逆转录酶)已被证明在细胞永生化过程中发挥作用。

方法

测定了11种头颈部鳞状细胞癌(SCCHN)细胞系中的端粒酶活性。通过重组腺病毒将野生型p16、p21、E2F-1和p53基因导入两种SCCHN细胞系,检测这些基因对端粒酶活性的影响。

结果

我们发现,在检测的11种SCCHN细胞系中有10种端粒酶活性升高。当我们用野生型p16、p21、E2F-1和p53基因感染Tu-138和Tu-167细胞系时,发现p16对端粒酶活性影响不大。已知E2F-1和p53均可诱导SCCHN细胞系凋亡。p53使两种细胞系的端粒酶活性显著降低,E2F-1使Tu-167细胞的端粒酶活性显著降低,这与细胞生长受抑制一致。p21的过表达也使端粒酶活性降低。

结论

我们从本研究得出结论,E2F-1和p53的过表达可逆转SCCHN细胞系中的端粒酶活性,且端粒酶活性可能参与癌细胞永生化。

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