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Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis

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机构: [1]Zunyi Med Univ, Dept Oncol, Affiliated Hosp, Zunyi, Peoples R China; [2]Guizhou Prov Peoples Hosp, Dept Oncol, Guiyang, Guizhou, Peoples R China; [3]Sun Yat Sen Univ, Canc Ctr, State Key Lab Oncol South China, Guangzhou, Guangdong, Peoples R China; [4]Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China; [5]Puer Univ, Puer, Peoples R China; [6]Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou, Guangdong, Peoples R China; [7]West Virginia Univ, Mary Babb Randolph Canc Inst, WVU Canc Inst, Robert C Byrd Hlth Sci Ctr, Morgantown, WV USA; [8]Guangzhou Med Univ, Affiliated Canc Hosp & Inst, 78 Hengzhigang Rd, Guangzhou, Guangdong, Peoples R China
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Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer-related death, especially in China. In addition, the prognosis of late stage patients is extremely poor. However, the biological significance of the long non-coding RNA lnc-ATB and its potential role in ESCC remain to be documented. In this study, we investigated the role of lnc-ATB and the underlying mechanism promoting its oncogenic activity in ESCC. Expression of lnc-ATB was higher in ESCC tissues and cell lines than that in normal counterparts. Upregulated lnc-ATB served as an independent prognosis predictor of ESCC patients. Moreover, loss-offunction assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC. Our results suggest that lnc-ATB predicts poor prognosis and may serve as a potential therapeutic target for ESCC patients.

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出版当年[2017]版:
大类 | 2 区 生物
小类 | 3 区 细胞生物学
最新[2023]版:
大类 | 1 区 生物学
小类 | 2 区 细胞生物学
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第一作者机构: [1]Zunyi Med Univ, Dept Oncol, Affiliated Hosp, Zunyi, Peoples R China;
通讯作者:
通讯机构: [3]Sun Yat Sen Univ, Canc Ctr, State Key Lab Oncol South China, Guangzhou, Guangdong, Peoples R China; [4]Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China; [8]Guangzhou Med Univ, Affiliated Canc Hosp & Inst, 78 Hengzhigang Rd, Guangzhou, Guangdong, Peoples R China
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