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Long non-coding RNA LINC00930 targeting miR-6792-3p/ZBTB16 regulates the proliferation and EMT of pancreatic cancer.
Mao, Yingqing; Su, Xian; Guo, Qingsong; Yao, Xihao; Zhao, Qun; Guo, Yibing; Wang, Yao; Li, Xiaohong; Lu, Yuhua.
Afiliación
  • Mao Y; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
  • Su X; The Sixth People's Hospital of Nantong, Nantong, 226001, P. R. China.
  • Guo Q; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
  • Yao X; Department of Hepatobiliary Surgery, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200000, P. R. China.
  • Zhao Q; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
  • Guo Y; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
  • Wang Y; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
  • Li X; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
  • Lu Y; Research Center of Clinical Medical, Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, P. R. China.
BMC Cancer ; 24(1): 638, 2024 May 24.
Article en En | MEDLINE | ID: mdl-38789960
ABSTRACT
Emerging evidence suggests the dysregulation of long non-coding RNAs (lncRNAs) involved in pancreatic cancer (PC). However, the function of LINC00930 in PC has not been elaborated. In this study, we found that LINC00930 was significantly down-regulated in PC cell lines and tissues, and associated with tumor size, lymphatic metastasis, TNM stage and poor prognosis. According to the bioinformatics database, the downregulation of LINC00930 was a common event in PC associated with prognosis and EMT. Overexpression of LINC00930 inhibited the aggressive cancer phenotypes including proliferation, metastasis and epithelial-mesenchymal transition (EMT) of PC in vitro and in vivo. Bioinformatics and dual-luciferase reporter assay indicated that miR-6792-3p could directly bind to LINC00930. Additionally, the Zinc finger and BTB domain containing 16 (ZBTB16) was significantly declined in PC, which was predicted to be the downstream gene of miR-6792-3p. MiR-6792-3p mimic rescued the decreased proliferation, metastasis and EMT caused by ZBTB16 in PC cells. The LINC00930/miR-6792-3p/ZBTB16 axis was associated with the malignant progression and process of PC. The relative expression of LINC00930 was negatively correlated with the expression of miR-6792-3p and was closely linked with ZBTB16 levels in PC. LINC00930 might serve as a potential prognostic biomarker and therapeutic target for PC.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Regulación Neoplásica de la Expresión Génica / MicroARNs / Proliferación Celular / Transición Epitelial-Mesenquimal / ARN Largo no Codificante Límite: Animals / Female / Humans / Male / Middle aged Idioma: En Revista: BMC Cancer Asunto de la revista: NEOPLASIAS Año: 2024 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Regulación Neoplásica de la Expresión Génica / MicroARNs / Proliferación Celular / Transición Epitelial-Mesenquimal / ARN Largo no Codificante Límite: Animals / Female / Humans / Male / Middle aged Idioma: En Revista: BMC Cancer Asunto de la revista: NEOPLASIAS Año: 2024 Tipo del documento: Article