ABSTRACT
Objective:To investigate the effects and its mechanism of long non-coding RNA (LncRNA) small nucleolar RNA host gene 6 (SNHG6) on proliferation, apoptosis and chemosensitivity of prostate cancer stem cells.Methods:CD44 + CD24 - tumor stem cells and non-CD44 + CD24 - cells were selected from prostate cancer cell PC-3 by flow separation technology, and the expression level of SNHG6 and microRNA (miR) -26a were detected by real-time fluorescence quantitative PCR. Cell proliferation was detected by 5-bromodeoxyuridine (Br-dU) , the apoptosis was detected by flow cytometry, the chemosensitivity of cells to cisplatin was detected by methyl thiazolyl tetrazolium (MTT) , and Western blot was used to detect the protein expressions of proliferating cell nuclear antigen (Ki-67) , B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) ; moreover, the target relationships of SNHG6, miR-26a and zeste enhancer of zeste homolog 2 (EZH2) were detected by double luciferase reporter gene assay, and Western blot was used to detect the effect of miR-26a analog on EZH2 protein expression. Results:Compared with non-CD44 + CD24 - cells, the expression level of SNHG6 in CD44 + CD24 - cells was significantly higher ( P<0.05) ; compared with NC-siRNA group [ (1.00±0.06) %, (96.85±6.48) %, (0.72±0.06) %, (0.43±0.03) %, (5.32±0.15) %, (0.35±0.03) %], SNHG6 expression level (0.25±0.03) , cell proliferation activity [ (75.36±5.1) %], Ki67 (0.38±0.03) and Bcl-2 protein (0.21±0.02) expression levels in SNHG6-siRNA group were significantly lower, while miR-26a expression level, apoptosis rate [ (13.83±2.36) %] and Bax protein (0.48±0.03) expression level were significantly higher, and the sensitivity of the cells to cisplatin was significantly higher ( P<0.05) ; in addition, miR-26a was the target gene of SNHG6, EZH2 was the target gene of miR-26a, and miR-26a analog could reduce the expression level of EZH2 protein. Conclusions:SNHG6 is up-regulated in prostate cancer stem cells. Interfering SNHG6 expression can inhibit the proliferation of cancer stem cells, promote apoptosis, and enhance the sensitivity of cancer stem cells to cisplatin. The mechanism may be related to the targeting regulation of miR-26a/EZH2 axis.
ABSTRACT
<p><b>OBJECTIVE</b>To detect the ability of Enterococcus faecalis (E. faecalis) biofilm formation and explore the relationship between E. faecalis biofilm formation ability and clinical manifestation.</p><p><b>METHODS</b>96 well plate with the establishment of 53 E. faecalis in vitro biofilm model, combined with crystal violet staining, was used to test the biofilm formation ability of the clinical isolates E. faecalis and analyze the relationship between biofilm formation capacity and clinical manifestation.</p><p><b>RESULTS</b>In total 53 E. faecalis strains, 40 strains(75.47%) had biofilm forming ability. Statistical analysis revealed that the capacities of biofilm formation between E. faecalis isolated from with fistula and without fistula was significantly different (P<0.05).</p><p><b>CONCLUSION</b>In the retreatment of root canal, the ability of biofilm formation of E. faecalis separated from the teeth without fistula is better than those separated from the teeth with fistula.</p>