ABSTRACT
Purpose This study aimed to investigate the relationship between miR-141-3p and B lymphocyte-2 gene (Bcl2) gene and its biological behavior on colon cancer cell line SW480. Methods qRT-PCR was used to detect the expression level of miR-141-3p in colon cancer tissues and adjacent tissues, as well as in colon cancer cell line and normal human colonic epithelial cell line FHC. MTT assay, wound assay, and Transwell demonstrated the effects of miR-141-3p on colon cancer proliferation, migration and invasion. Targetscan7.1 predictive software and dual luciferase reporter assays were used to detect the targeted regulation of miR-141-3p on the apoptosis-related gene Bcl2. MTT assay, wound assay, Transwell and flow cytometry were used to detect the effect of Bcl2 on miR-141-3p on colon cancer proliferation, migration, invasion and apoptosis. Results Compared with adjacent tissues, the expression of miR-141-3p in colon cancer tissues was significantly down-regulated. Colon cancer patients with low expression of miR-141-3p had poorer prognosis. Compared with normal colonic epithelial cells, miR-141-3p expression was significantly down-regulated in colon cancer cell lines, and overexpression of miR-141-3p significantly attenuated the proliferation, migration and invasion of colon cancer cells. Knockdown of miR-141-3p significantly promoted the proliferation, migration and invasion of colon cancer cells. miR-141-3p targets the negative regulation of Bcl2. Knockdown of Bcl2 significantly attenuated the promotion of miR-141-3p inhibitor on proliferation, migration and invasion of colon cancer cells and inhibition of apoptosis. Knockdown of Bcl2 significantly enhanced the inhibition effect of miR-141-3p inhibitor on proliferation, migration and invasion of colon cancer cells. Conclusions In conclusion, miR-141-3p can inhibit the cancer by regulating Bcl2, and miR-141-3p has the potential to become a potential therapeutic target for colon cancer (AU)
Subject(s)
Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Gene Expression Regulation, Neoplastic , Colonic Neoplasms/metabolism , Colonic Neoplasms/pathology , MicroRNAs/genetics , Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors , Apoptosis , Cell Movement , Cell Proliferation , Colonic Neoplasms/genetics , Neoplasm Invasiveness , Prognosis , Genes, bcl-2/genetics , Survival Analysis , Tumor Cells, CulturedABSTRACT
PURPOSE: This study aimed to investigate the relationship between miR-141-3p and B lymphocyte-2 gene (Bcl2) gene and its biological behavior on colon cancer cell line SW480. METHODS: qRT-PCR was used to detect the expression level of miR-141-3p in colon cancer tissues and adjacent tissues, as well as in colon cancer cell line and normal human colonic epithelial cell line FHC. MTT assay, wound assay, and Transwell demonstrated the effects of miR-141-3p on colon cancer proliferation, migration and invasion. Targetscan7.1 predictive software and dual luciferase reporter assays were used to detect the targeted regulation of miR-141-3p on the apoptosis-related gene Bcl2. MTT assay, wound assay, Transwell and flow cytometry were used to detect the effect of Bcl2 on miR-141-3p on colon cancer proliferation, migration, invasion and apoptosis. RESULTS: Compared with adjacent tissues, the expression of miR-141-3p in colon cancer tissues was significantly down-regulated. Colon cancer patients with low expression of miR-141-3p had poorer prognosis. Compared with normal colonic epithelial cells, miR-141-3p expression was significantly down-regulated in colon cancer cell lines, and overexpression of miR-141-3p significantly attenuated the proliferation, migration and invasion of colon cancer cells. Knockdown of miR-141-3p significantly promoted the proliferation, migration and invasion of colon cancer cells. miR-141-3p targets the negative regulation of Bcl2. Knockdown of Bcl2 significantly attenuated the promotion of miR-141-3p inhibitor on proliferation, migration and invasion of colon cancer cells and inhibition of apoptosis. Knockdown of Bcl2 significantly enhanced the inhibition effect of miR-141-3p inhibitor on proliferation, migration and invasion of colon cancer cells. CONCLUSIONS: In conclusion, miR-141-3p can inhibit the cancer by regulating Bcl2, and miR-141-3p has the potential to become a potential therapeutic target for colon cancer.
Subject(s)
Biomarkers, Tumor/metabolism , Colonic Neoplasms/pathology , Gene Expression Regulation, Neoplastic , MicroRNAs/genetics , Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors , Apoptosis , Biomarkers, Tumor/genetics , Cell Movement , Cell Proliferation , Colonic Neoplasms/genetics , Colonic Neoplasms/metabolism , Humans , Neoplasm Invasiveness , Prognosis , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , Survival Rate , Tumor Cells, CulturedABSTRACT
OBJECTIVE: The aim of the study was to explore the association between F-box and leucine-rich repeat protein 19-antisense ribonucleic acid 1 (FBXL19-AS1) and acute pancreatitis (AP) and its role in prognostic evaluation. PATIENTS AND METHODS: According to the severity of AP, the patients were classified into mild group, moderate-severe group, and severe group, and the expression of FBXL19-AS1 was compared among the three groups. The associations of FBXL19-AS1 with Atlanta classification, computed tomography severity index (CTSI), acute physiology and chronic health evaluation (APACHE) II score, bedside index for severity in acute pancreatitis (BISAP) and Ranson score were analyzed. The optimal cut-off point of severe hyperlipidemia-induced AP was predicted by the receiver operating characteristic (ROC) curves. Then, the incidence rates of local and systemic complications were compared among AP patients with different levels of FBXL19-AS1. After overexpression of FBXL19-AS1 in AP cells, the quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) results showed that significantly upregulated the mRNA level of interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), and IL-6. The opposite results were obtained after the knockdown of FBXL19-AS1 in cells. RESULTS: There were no statistical differences in the basic data among the three groups. The FBXL19-AS1 level was increased in severe group than the moderate-severe group and mild group. The area under the curve (AUC) of FBXL19-AS1 in predicting severe AP was 0.9177 (p<0.001). According to the Spearman correlation analysis, the FBXL19-AS1 level had significant positive correlations with the predictive scores of AP severity. The incidence rate of shock, liver dysfunction, and pancreatic necrotic tissue infection was significantly higher in FBXL19-AS1 high-expression group than that in FBXL19-AS1 low-expression group. FBXL19-AS1 could promote the upregulation of inflammatory indexes. CONCLUSIONS: FBXL19-AS1 is highly expressed in the serum of AP patients, and it is positively correlated with the severity of AP. FBXL19-AS1 mediates the inflammatory response and promotes the occurrence and development of pancreatitis, harming the prognosis of patients.
