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LncRNA-UCA1 exerts oncogenic functions in non-small cell lung cancer by targeting miR-193a-3p.
Nie, Wei; Ge, Hui-juan; Yang, Xiao-qun; Sun, Xiangjie; Huang, Hai; Tao, Xia; Chen, Wan-sheng; Li, Bing.
Affiliation
  • Nie W; Department of Respiratory Medicine, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
  • Ge HJ; Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
  • Yang XQ; Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
  • Sun X; Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
  • Huang H; Department of Respiratory Medicine, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
  • Tao X; Department of Pharmacy, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
  • Chen WS; Department of Pharmacy, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. Electronic address: chenws126@126.com.
  • Li B; Department of Respiratory Medicine, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. Electronic address: bing_li1962@163.com.
Cancer Lett ; 371(1): 99-106, 2016 Feb 01.
Article in En | MEDLINE | ID: mdl-26655272
ABSTRACT
Recently, the long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been identified as an oncogenic gene in multiple human tumor entitles, and dysregulation of UCA1 was tightly linked to carcinogenesis and cancer progression. However, whether the aberrant expression of UCA1 in non-small cell lung cancer (NSCLC) is associated with malignancy, metastasis or prognosis has not been characterized. In this study, we found that UCA1 was upregulated in NSCLC tissues. Higher expression of UCA1 led to a significantly poorer survival time, and multivariate analysis revealed that UCA1 was an independent risk factor of prognosis. UCA1 overexpression enhanced, whereas UCA1 silencing impaired the proliferation and colony formation of NSCLC cells. Moreover, mechanistic investigations showed that UCA1 upregulated the expression of miR-193a-3p target gene ERBB4 through competitively 'spongeing' miR-193a-3p. Overall, we concluded that UCA1 functions as an oncogene in NSCLC, acting mechanistically by upregulating ERBB4 in part through 'spongeing' miR-193a-3p.
Subject(s)
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oncogenes / Carcinoma, Non-Small-Cell Lung / MicroRNAs / RNA, Long Noncoding / Lung Neoplasms Type of study: Etiology_studies / Observational_studies / Prognostic_studies Limits: Female / Humans / Male / Middle aged Language: En Journal: Cancer Lett Year: 2016 Document type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oncogenes / Carcinoma, Non-Small-Cell Lung / MicroRNAs / RNA, Long Noncoding / Lung Neoplasms Type of study: Etiology_studies / Observational_studies / Prognostic_studies Limits: Female / Humans / Male / Middle aged Language: En Journal: Cancer Lett Year: 2016 Document type: Article Affiliation country: China