Selected article for: "expression level and real time"

Author: Zheng, D-N; Zhang, C-J; Sun, G-P
Title: Long non-coding RNA MNX1-AS1 promotes migration and invasion of esophageal squamous cell carcinoma by upregulating IGF2.
  • Cord-id: 37rrlzmo
  • Document date: 2019_1_1
  • ID: 37rrlzmo
    Snippet: OBJECTIVE Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor with a high mortality rate and poor prognosis. In this research, we investigated the exact role of long non-coding ribonucleic acids (lncRNA) MNX1-AS1 in the metastasis of ESCC and its possible mechanism. PATIENTS AND METHODS To investigate the functions of MNX1-AS1 in ESCC, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect MNX1-AS1 expression of ESCC tissues and cells. Besides, functi
    Document: OBJECTIVE Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor with a high mortality rate and poor prognosis. In this research, we investigated the exact role of long non-coding ribonucleic acids (lncRNA) MNX1-AS1 in the metastasis of ESCC and its possible mechanism. PATIENTS AND METHODS To investigate the functions of MNX1-AS1 in ESCC, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect MNX1-AS1 expression of ESCC tissues and cells. Besides, functional assays, including transwell assay and wound healing assay, were performed. Furthermore, qRT-PCR and Western blot assay were used to explore the possible underlying regulatory mechanism. RESULTS The expression level of MNX1-AS1 was significantly increased in both ESCC tissues sample and cells. Moreover, knockdown of MNX1-AS1 markedly inhibited the migration and invasion of ESCC cells. Besides, knockdown of MNX1-AS1 remarkably down-regulated the mRNA and protein levels of insulin-like growth factor 2 (IGF2). Furthermore, IGF2 expression was positively correlated with MNX1-AS1 expression in ESCC tissues. CONCLUSIONS MNX1-AS1 serves as a potential oncogene in ESCC, which can significantly promote ESCC cell migration and invasion by up-regulating IGF2. Our findings may provide a new therapeutic target of ESCC.

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