Abstract
Long non-coding RNA associated with poor prognosis of hepatocellular carcinoma (lncRNA-AWPPH) is a newly discovered lncRNA that has important functions in the pathogenesis of several malignancies. However, its role in the development of colorectal adenocarcinoma is unknown. The current study therefore investigated the function of AWPPH in colorectal adenocarcinoma. A total of 86 patients with colorectal adenocarcinoma and 56 healthy controls were included. Tumor tissues and adjacent healthy tissues were collected from patients with colorectal adenocarcinoma, and blood was collected from both patients and healthy controls. Expression of AWPPH in tissues and blood was detected by the reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curve analysis was used to evaluate the diagnostic value of serum AWPPH for colorectal adenocarcinoma. All patients were followed up for 5 years, and survival curve analysis was performed to investigate the association between serum level of AWPPH and patients' survival. The effects of AWPPH overexpression and silencing in colorectal adenocarcinoma cell lines were investigated. Effects on cell proliferation and viability were detected by the cell counting kit-8 and MTT assays, respectively. Effects on transforming growth factor β1 (TGF-β1) expression were determined by western blotting. AWPPH was significantly upregulated in tumor tissues compared with adjacent healthy tissues. AWPPH expression levels in blood increased in patients with colorectal adenocarcinoma compared with healthy controls, suggesting that AWPPH may be a sensitive and accurate diagnostic and prognostic biomarker for colorectal adenocarcinoma. AWPPH overexpression in colorectal adenocarcinoma cell lines promoted cell proliferation and increased cell viability, while AWPPH silencing resulted in opposite effects. AWPPH overexpression promoted and silencing inhibited TGF-β1 expression. Therefore, lncRNA-AWPPH promoted colorectal adenocarcinoma by promoting tumor growth, increasing tumor cell viability and activating the TGF-β1 signaling.