ABSTRACT
BACKGROUND AND OBJECTIVE: Long non-coding RNA, BANCR, has been demonstrated to contribute to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer is still unknown. In present study, we investigated whether BANCR was involved in the development of gastric cancer cells via regulation of NF-κB1. METHODS: Human gastric cancer tissues were isolated as well as human gastric cell lines MGC803 and BGC823 were cultured to investigate the role of BANCR in gastric cancer. RESULTS: BANCR expression was significantly up-regulated in gastric tumor tissues and gastric cell lines. Down-regulation of BANCR inhibited gastric cancer cell growth and promoted cell apoptosis, and it also contributed to a significant decrease of NF-κB1 (P50/105) expression and 3'UTR of NF-κB1 activity. Overexpression of NF-κB1 reversed the effect of BANCR on cancer cell growth and apoptosis. MiroRNA-9 (miR-9) targeted NF-κB1, and miR-9 inhibitor also reversed the effects of BANCR on gastric cancer cell growth and apoptosis. CONCLUSION: BANCR was highly expressed both in gastric tumor tissues and in cancer cells. NF-κB1 and miR-9 were involved in the role of BANCR in gastric cancer cell growth and apoptosis.
Subject(s)
Adenocarcinoma/genetics , Gene Expression Regulation, Neoplastic , MicroRNAs/genetics , NF-kappa B/genetics , RNA, Long Noncoding/genetics , Stomach Neoplasms/genetics , 3' Untranslated Regions , Adenocarcinoma/metabolism , Adenocarcinoma/pathology , Animals , Apoptosis , Cell Line, Tumor , Cell Proliferation , Humans , Mice , Mice, Nude , MicroRNAs/antagonists & inhibitors , MicroRNAs/metabolism , NF-kappa B/antagonists & inhibitors , NF-kappa B/metabolism , Neoplasm Transplantation , Proto-Oncogene Proteins B-raf/genetics , Proto-Oncogene Proteins B-raf/metabolism , RNA, Long Noncoding/antagonists & inhibitors , RNA, Long Noncoding/metabolism , RNA, Small Interfering/genetics , RNA, Small Interfering/metabolism , Signal Transduction , Stomach Neoplasms/metabolism , Stomach Neoplasms/pathologyABSTRACT
BACKGROUND: This study is to explore the pathological features of transplanted tumor established by CD133 positive TJ905 glioblastoma stem-like cells. METHODS: CD133 positive TJ905 glioma cells were separated by immunomagnetic beads to isolate glioma stem-like cells. TJ905 cells and stem-like cells were inoculated subcutaneously into the mice to establish model of transplanted tumor, respectively. Mice growing condition and behavior were observed. HE staining assay, immunohistochemical assay for GFAP, Ki-67 and Olig-2, and CD34 marked microvascular density (MVD) test were performed. RESULTS: The growing condition and behavior of mice in TJ905 stem cell group was more exaggerated and the models showed stronger malignant features pathologically than that in TJ905 cell group. Glial fibrillary acidic protein (GFAP) in TJ905 cell and stem-like cell group showed the transplanted tumor originated from astrocytes. Expression of Ki-67 and oligodendrocyte transcription factor-2 (Olig-2) in TJ905 stem cells was higher notably and CD34 expression in stem cell group was significantly higher than that in the other two groups. CONCLUSIONS: Pathological features of transplanted tumor established by CD133 positive glioblastoma stem-like cells show more malignant. Use of TJ905 stem cells to establish transplanted tumor model in nude mice is excellent for glioma research.
ABSTRACT
OBJECTIVE: Our study aims at assessing the association between miR-30a along with its target gene snail 1 and atrial fibrillation (AF)-induced myocardial fibrosis. METHODS: Ang II was used to up-regulate cardiac fibroblasts fibrosis in vitro, and then the cardiac fibroblasts were divided into the mimics group (mimics miR-30a), inhibitors group (inhibitors miR-30a), NC group (transfected miR-30a, negative control) and blank control group (non-transfected cells). Two-group (sham operated group and rapid pacing group) AF rabbit models were constructed according to whether rapid pacing was presented in the subject. Then the establishment of rabbit models was examined using histopathology after Masson staining. The mRNA and protein expression levels of snail 1 and periostin in cardiac fibroblasts and myocardial tissues were detected using the method of RT-PCR and Western blot, respectively. RESULTS: In vitro, our experiment showed that overexpression of miR-30a in cardiac fibroblasts contribute to a significant decrease in the average expression level of snail 1 and periostin (P < 0.05) whereas inhibition of miR-30a significantly increased the average expression level of snail 1 and periostin (P < 0.05). In vivo, the average expression level of miR-30a significantly decreased in myocardial tissues with an increased degree of myocardial fibrosis, while the snail 1 and periostin expression level significantly increased during a certain period of time (P < 0.05). CONCLUSION: Our results suggest that miR-30a target snail 1 protein may be related to AF-induced myocardial fibrosis. The average expression levels of snail 1 increased significantly in both myocardial cells and tissues, while miR-30a could inhibit the expression of snail 1. Thus, we speculate that miR-30a and snail 1 may be potential therapeutic targets for curing AF-induced myocardial fibrosis.
