RESUMO
Objective Long non-coding RNA(lncRNA) are aberrantly expressed in breast cancer(BC) and strongly associated with its survival prognosis. The aim of this study is to investigate the expression and effect of IncRNA SPATA31D5P on the invasion and migration capacity of breast cancer cells through adsorption of miR-320a. Methods Totally 30 cases of BC tissues and paraneoplastic tissues were collected, and the expression levels of SPATA31D5P in BC tissues and BC cell lines were detected by Real-time PCR. MDA-MB-231 cells were transfected with SPATA31D5P siRNA interference vector, and cell proliferation, invasion and migration capacity were determined using the cell counting kit-8 assay (CCK-8), 5-ethynyl-2'- deoxyuridine(EdU), Transwell and wound-healing assay respectively. And cell cycle and apoptosis were detected by flow cytometry. Bioinformatics approachs were used to screen for miRNAs that could bind complementarily to SPATA31D5P, and the regulatory effect of SPATA31D5P on miR-320a was detected by Real-time PCR and dual luciferase reporter assay. Results SPATA31D5P levels were significantly higher in BC tissues than in adjacent normal breast tissues, and SPATA31D5P expression was higher in each BC cell line than in normal breast epithelial cells MCF10 A. The level of SPATA31D5P in the interference group was 0. 288±0. 052, which was lower than that of the blank control group 1. 114±0. 096 and negative control (NC) group 1. 079±0. 128 (P< 0. 01). The proliferation activity of MDA- MB-231 cells in the interfered group was significantly reduced and apoptotic rate was obviously increased compared to the NC and control groups (P<0. 01) ;the Gj phase block was observed in the interfered group; the scratch healing rate and number of perforated cells in the interference group were (14. 36 ± 1. 75) % and (26±1.52), which were lower than (52. 25± 1.87)% and ( 67. 33 ± 2. 91 ) of the NC group (PcO.Ol). Dual luciferase experiments confirmed that SPATA31D5P could directly regulate miR-320a expression and luciferase activity. Conclusion SPATA31D5P is highly expressed in BC, interfering with SPATA31D5P expression effectively inhibits the proliferation, migration and invasion of MDA-MB-231 cells, and the mechanism may be related to the targeted regulation of miR-320a.
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Objective The purpose of this study is to investigate the expression of the polypeptide N-acetylgalactosaminyltransferase-10 (ppGalNAc-T10) protein in lung and breast and colon cancer. Methods Immunohistochemistry was used to analyse ppGalNAc-T10 expressions in 110 lung cancer tissues, 100 breast cancer tissues and 110 colon cancer tissues. Meanwhile, different cancer has 10 cases of normal tissues as control. Results The expression of ppGalNAc-T10 in normal lung tissue was higher compared with that in lung cancer organizations, and ppGalNAc-T10 positive expression was found to be significantly associated with invasion depth of tumor (P < 0. 01). PpGalNAc-T10 protein expression in breast and colon cancer was no significantly difference than that in non-tumor breast and colon tissue. Conclusion PpGalNAc-T10 expression is a useful marker in lung cancer.
RESUMO
<p><b>OBJECTIVE</b>To explore the effects of silencing HERC4 on the proliferation, apoptosis, and migration of cervical cancer cell line Hela and the possible molecular mechanisms.</p><p><b>METHODS</b>Three HERC4-specific small interfering RNAs (siRNAs) were transfected into Hela cells, and HERC4 expression in the cells was examined with Western blotting. CCK-8 assay, annexin V-FITC/PI assay, and wound healing assay were used to assess the effect of HERC4 silencing on the proliferation, apoptosis and migration ability of Hela cells. The expression levels of cyclin D1 and Bcl-2 in the cells were detected using Western blotting.</p><p><b>RESULTS</b>Transfection of siRNA-3 resulted in significantly decreased HERC4 protein expression (P<0.01). HERC4 silencing by siRNA-3 markedly suppressed the proliferation and migration of Hela cells, increased the apoptosis rate (P<0.01) and reduced the expression levels of cyclin D1 and Bcl-2 (P<0.01).</p><p><b>CONCLUSION</b>Silencing of HERC4 efficiently inhibits the proliferation, migration, and invasion of Hela cells in vitro, and the underlying mechanisms may involve the down-regulation of cyclin D1 and Bcl-2.</p>