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OBJECTIVE: The aim of this study is to investigate the expression levels of circRNA_100782 in gastric cancer tissues, and its function of regulating tumor suppressor gene Rb by absorbing miR-574-3p in a sponge form. PATIENTS AND METHODS: qRT-PCR was performed to detect the expressions of circRNA_ 100782 at different stages during gastric cancer tissues. CCK-8 assay was performed to evaluate the osteoclast proliferation and differentiation. The correlation between miR-574-3p and circRNA_100782 was detected by statistical analysis. Bioinformatics and Luciferase assay were performed to explore the interaction and binding site of circRNA_100782 and miR- 574-3p. The mice Rb 3′-UTR were cloned into the Luciferase reporter vector and miR-574-3p binding mutants were constructed to validate the inhibited regulation of miR-574-3p to the expression of Rb. RESULTS: In the current study, compared with adjacent non-cancerous normal tissues, the expressions of circRNA_100782 and Rb were both downregulated in human gastric cancer cells. Through qRT-PCR and CCK-8 assay, we found that the expression of circRNA_100782 is related to the proliferation of gastric cancer cells. Besides, we also found that circRNA_100782 regulated the migration ability of gastric cancer cells through transwell assay. The bioinformatics prediction and luciferase assay demonstrated that circRNA_100782 can serve as a molecular sponge to further regulate the expression of Rb by sponging with miR-574-3p; moreover, circRNA_ 100782 can serve as a ceRNA for miR- 574-3p to further regulate the expression of Rb. CONCLUSIONS: In this research, we discovered that circRNA_100782 was downregulated in gastric cancer cells and is associated with cell proliferation and invasion by inhibiting tumor suppressor gene Rb by interacting with miR-574-3p. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the role of long non-coding RNA Cancer Susceptibility Candidate 15 (CASC15) in cervical cancer and its potential molecular mechanism. PATIENTS AND METHODS: The CASC15 expression was measured in cervical cancer tissues and cell lines by using quantitative Real-time polymerase chain reaction (qRT-PCR) analysis. Cell counting kit-8 (CCK8), flow cytometry analysis and transwell cell invasion assays were employed to detect the capacities of cell proliferation and cell invasion. Furthermore, Western blot analysis was applied to detected the E-cadherin and N-cadherin expression in EMT pathway. RESULTS: We demonstrated that lncRNA CASC15 expression was higher in cervical cancer tissues compared to adjacent normal tissues. Higher lncRNA CASC15 expression associated with lymph node metastasis and FIGO stage. Moreover, our results showed that higher lncRNA CASC15 expression predicted poor prognosis of cervical cancer. Functional assays showed that knockdown of lncRNA CASC15 suppressed cell proliferation and cell cycle progression in cervical cancer. Moreover, we also found that knockdown of lncRNA CASC15 inhibited cell invasion ability and Epithelial-Mesenchymal Transition (EMT) signaling pathway by upregulating E-cadherin and downregulating N-cadherin expression in cervical cancer. CONCLUSIONS: These results indicated that lncRNA CASC15 expression may be a prognostic biomarker and contributed to cell proliferation and invasion in cervical cancer. [ABSTRACT FROM AUTHOR]

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Schisandrin B is an active monomer of the Chinese magnolia vine (Schisandra chinensis) that can reduce transaminase activity in liver cells, inhibit lipid peroxidation, enhance antioxidant status, has protective effects in the liver and has antitumor effects. The present study investigated the potential protective effects of schisandrin B on the p53 signaling pathway in attenuating the inflammatory response, oxidative stress and apoptosis induced by traumatic spinal cord injury (TSCI) in adult rats. Behavioral examination, inclined plate test and spinal cord water content were used to evaluate the protective effect of schisandrin B in TSCI rats. The expression levels of superoxide dismutase (SOD), malondialdehyde (MDA), nuclear factor (NF)-κB subunit p65 and tumor necrosis factor (TNF)-α were examined using ELISA kits. Western blot analysis was performed to analyze the protein expression of caspase-3 and phosphorylated (p)-p53 in TSCI rats. In the present study, schisandrin B improved behavioral examination results and the maximum angle of inclined plate test, and inhibited spinal cord water content in rats with TSCI. Notably, schisandrin B reduced the activation of traumatic injury-associated pathways, including SOD, MDA, NF-κB p65 and TNF-α, in TSCI rats. In addition, schisandrin B suppressed the TSCI-induced expression of caspase-3 and p-p53 in TSCI rats. These results indicated that schisandrin B may attenuate the inflammatory response, oxidative stress and apoptosis in TSCI rats by inhibiting the p53 signaling pathway in adult rats. [ABSTRACT FROM AUTHOR]

Purpose: To explore the sensitization of suberoylanilide hydroxamic acid (SAHA) on chemoradiation for cervical cancer cells and its mechanism. Materials and Methods: After human cervical cancer SiHa cells were treated with SAHA and cisplatin (DDP) of different concentrations, inhibition and apoptosis rates, and cell cycle were detected. SiHa cells underwent radiation of various doses after treated with 20% IC50 of SAHA for 24 hours. The survival fraction of SiHa cells was calculated by colony-forming assay, and related parameters were calculated. mRNA and protein expressions of P21, Bax and Ku70 were detected. Results: The inhibition rate was higher in SD (SAHA combined with DDP) group than in D (DDP alone) group (p < 0.05). The number of cells in G0/G1 phase was higher, and the number of cells in G2/M+S phase and PI (proliferation index) were lower in S (SAHA), D, and SD groups than in control group, and in SD group than in S and D groups (p < 0.05). The apoptosis rate and the expressions of mRNA and protein of Bax and P21 were higher in SD group than in S or D group (p < 0.05). The cell survival fraction was lower in SAHA combined with radiotherapy group than in radiotherapy alone group (p < 0.05). Do, N, and Dq values were 2.329, 2.761, and 1.721, respectively, in radiotherapy alone group and 1.213, 4.770, and 0.823, respectively, in SAHA combined with radiotherapy group. SER was 1.92. Bax mRNA and protein expressions were higher but Ku70 mRNA and protein expressions were lower in SAHA combined with radiotherapy group than in radiotherapy alone group (p < 0.05). Conclusion: SAHA promotes SiHa apoptosis in chemotherapy through up-regulation of mRNA and protein of p21 and Bax which leads to cell cycle arrest in G0/G1 phase. Low dose of SAHA promotes SiHa apoptosis and inhibits cell repair in radiotherapy through Bax up-regulation and Ku70 down-regulation. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To determine whether autophagy was involved in chondrocyte cells post Glucocorticoids (GCs) treatment. MATERIALS AND METHODS: LC3-GFP reporter plasmid transfection and western blotting analysis were conducted to determine the autophagic vesicles and autophagy-associated molecules in the N1511 chondrocyte cells post dexamethasone (Dex) treatment. And the N1511 cell viability was also determined by MTT assay. RESULTS: We found that autophagy was induced in the N1511 chondrocyte cells post treatment with Dex of 5 µM to 1 mM, and the autophagy-induction by Dex could be inhibited by 3 MA and RU486, a GC antagonist. And the autophagy induced by the high dose of Dex (200 µM or 1 mM) was associated with a reduction of N1511 cell viability. CONCLUSIONS: These results suggested that GCs could induce autophagy, as might contribute to the viability reduction of chondrocyte cells. [ABSTRACT FROM AUTHOR]

Tumor metastasis remains the major cause of cancer-related death, but its molecular basis is still not well understood. Here we uncovered a splicing-mediated pathway that is essential for breast cancer metastasis. We show that the RNA-binding protein heterogeneous nuclear ribonucleoprotein M (hnRNPM) promotes breast cancer metastasis by activating the switch of alternative splicing that occurs during epithelial-mesenchymal transition (EMT). Genome-wide deep sequencing analysis suggests that hnRNPM potentiates TGFβ signaling and identifies CD44 as a key downstream target of hnRNPM. hnRNPM ablation prevents TGFβ-induced EMT and inhibits breast cancer metastasis in mice, whereas enforced expression of the specific CD44 standard (CD44s) splice isoform overrides the loss of hnRNPM and permits EMT and metastasis. Mechanistically, we demonstrate that the ubiquitously expressed hnRNPM acts in a mesenchymal-specific manner to precisely control CD44 splice isoform switching during EMT. This restricted cell-type activity of hnRNPM is achieved by competition with ESRP1, an epithelial splicing regulator that binds to the same cis-regulatory RNA elements as hnRNPM and is repressed during EMT. Importantly, hnRNPM is associated with aggressive breast cancer and correlates with increased CD44s in patient specimens. These findings demonstrate a novel molecular mechanism through which tumor metastasis is endowed by the hnRNPM-mediated splicing program. [ABSTRACT FROM AUTHOR]

BACKGROUND: A harm reduction NGO in southern Yunnan operating an emergency overdose response hotline service successfully reversed 76 overdoses through the administration of naloxone in one of the first interventions of its kind in China. METHOD: To explore local understandings of risk factors related to overdose, assess ongoing barriers to overdose response, and solicit client input on how to further reduce opiate overdose mortality in Gejiu, the authors conducted qualitative interviews with 30 clients, including 15 individuals who received naloxone injections to reverse an overdose and 15 individuals who called the hotline in response to the overdose of a peer. RESULTS: Participants pointed to a number of local structural shifts in heroin use including the ageing of the opiate using population and drug mixing practises that contribute to the city's overdose toll. Concerns over medical professionals' willingness to treat drug users, protection of confidentiality, and financial costs associated with treatment frequently cause drug users to avoid contact with the city's emergency service providers. Participants suggest directly distributing naloxone to clients as one strategy to further reduce overdose mortality. CONCLUSION: The authors explore possible strategies, including targeted trainings and new partnerships with local hospitals, to further reduce opiate overdose mortality in this resource-poor setting. [ABSTRACT FROM AUTHOR]