Telomerase inhibition decreases esophageal squamous carcinoma cell migration and invasion

被引:6
作者
Li, Jiayan [1 ]
Dong, Guogang [2 ]
Song, Jinyun [1 ]
Tan, Guolei [1 ]
Wu, Xuping [1 ]
机构
[1] Nanjing Univ Chinese Med, Hosp Nanjing 2, 1-1 Zhongdu Rd, Nanjing 210003, Jiangsu, Peoples R China
[2] Gen Hosp Eastern Theater Command Chinese Peoples, Nanjing 210002, Jiangsu, Peoples R China
关键词
ESCC; telomerase; migration; invasion; prognosis; TERT PROMOTER MUTATIONS; DNA METHYLATION; CANCER INVASION; EXPRESSION; GROWTH; OCCUR; RISK; CARCINOGENESIS; PROLIFERATION; GLIOMAS;
D O I
10.3892/ol.2020.11810
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Telomerase has been shown to be associated with a variety of cancer types. To elucidate the role of telomerase in esophageal squamous carcinoma (ESCC), tissue samples from 100 patients with ESCC, and paired paracancerous tissues from 75 of these patients, were collected for use in the present study. Using immunohistochemical analysis, the expression of telomerase reverse transcriptase (hTERT) in the cytoplasm of ESCC cells was revealed to be significantly higher compared with that in paracancerous tissues, and no significant difference was observed between hTERT expression in the nucleus of ESCC and paracancerous tissue cells. Combined analysis revealed that the cytoplasmic hTERT-positive rate of patients with ESCC was significantly associated with pathological grade, N stage and Tumor-Node-Metastasis (TNM) stage; these data support the association between hTERT expression and poor patient prognosis.In vitroexperiments demonstrated that hTERT knockdown does not inhibit the proliferation of ESCC Kyse410 or Kyse520 cells, but inhibits their migration and invasion abilities. These findings indicate that hTERT expression is associated with ESCC metastasis. Interestingly, decreased colony-formation ability was observed in Kyse410 cells, but not in Kyse520 cells. Collectively, the results of the present study suggest that hTERT may serve as a potential therapeutic target for ESCC.
引用
收藏
页码:2870 / 2880
页数:11
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