Objective: To study the expression of miR-142-5p in lung adenocarcinoma tissues, and to explore its effect on proliferation, invasion, migration and epithelieal-mesenchymal transition (EMT) of H1650 cells and the potential mechanisms. Methods:Atotal of 107 pairs of lung adenocarcinoma tissues and corresponding para-cancerous tissues from patients, who underwent tumor resection and were pathologically confirmed at the Department of Thoracic Surgery, the Fourth Hospital of Hebei Medical University between Jan. 2014 and Jan. 2015, were collected for this study; in addition, human lung adenocarcinoma cell lines (H1650, HCC827, A549, H1975, PC9) and human bronchial epithelial BEAS-2B cells were also used in this study. qPCR was used to detect the expression of miR-142-5p in lung adenocarcinoma tissues and cell lines. The correlation between expression of miR-142-5p and clinical features was analyzed.After transfection with miR-142-5p mimics or miR-negative control (miR-NC) plasmid, the proliferation, invasion and migration of H1650 cells were detected with CCK-8, Transwell invasion assay and Wound healing assay, respectively. The bioinforamtics tool was used to predict the target genes of miR-142-5p, and Luciferase reporter gene assay was performed to validate the regulation of miR-142-5p on target gene. Western blotting (WB) was used to detect the expressions of cyclin-dependent kinase 5 (CDK5) and EMTrelated protein. Results: Compared to Para-cancerous tissues and BEAS-2B cells, the expression of miR-142-5p was lower in lung adenocarcinoma tissues and cell lines (all P<0.01). Of the 107 cases of lung adenocarcinoma tissues, 61 cases (57.01%) showed decreased miR-142-5 expression, which was correlated with the TNM stage and lymph node metastasis (both P<0.01). Transfection of miR-142-5p mimics significantly up-regulated the expression of miR-142-5p and decreased the proliferation, invasion and migration of H1650 cells (all P<0.05 or P<0.01). Bioinformatics showed that CDK5 was a target gene of miR-142-5p. Luciferase reporter gene assay and WB validated that miR-142-5p could significantly down-regulate CDK5 expression in H1650 cells, up-regulate the expression of E-cadherin and down-regulate the expressions of N-cadherin, Twist and Snail in H1650 cells (all P<0.01). Conclusion: miR-142-5p is low expressed in lung adenocarcinoma tissues and cell lines; it suppresses the EMT process to inhibit, invasion and migration of H1650 cells via down-regulating the expression of CDK5.

Objective: To investigate the effect of sulforaphane (SFN) on CD8+ T cells differentiation, phenotype and the secretion of intracellular cytokines, as well as to study the underlying molecular mechanism. Methods: In the in vitro culture experiment, the cells were categorized into control group, SNF 10 mmol/L group and SNF 20 mmol/L group according to the SNF concentration. The effect of SFN treatment on CD8+ T cells differentiation, phenotype and cytokine secretion were detected by flow cytometry, and the effect of mTOR siRNA on the expression of CD127 and LKRG1 in CD8+T cells was also detected by flow cytometry. Expression of Bcl-2 and Bcl-6 were analyzed by qRT-PCR. The effect of SFN on apoptosis of CD8+T cells was examined byAnnexin-V/PI staining. The protein expressions of p-mTOR, p-S6 and b-actin were detected by western blotting. Results: SFN significantly promoted the formation of memory precursor CD8+ T cells and decreased the expression level of PD-1 and Tim-3 in CD8+T cells(P<0.01); meanwhile, after the treatment of SFN, the expressions of anti-apoptosis genes Bcl-2 and Bcl-6 were significantly increased while the apoptosis of CD8+ T cells was significantly inhibited and the protein expressions of p-mTOR and p-S6 were also significantly inhibited(P<0.05 or P<0.01). Moreover, mTOR siRNA could significantly increasethe expression of CD127 and decrease the expression of LKRG1 (all P<0.01). Conclusion: Sulforaphone promotes the formation of memory precursor CD8+T cells possibly by inhibiting the p-mTOR signaling pathway, and this could obtain more T cells to provide new thoughts for clinical immunotherapy.

Objective: To explore the roles and mechanisms of long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) in promoting invasion and metastasis of esophageal squamous carcinoma (ESCC). Methods: Real time quantitative polymerase chain reaction (qPCR) was used to detect the expression of SNHG6 in ESCC and matched para-carcinoma tissues. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect the expression of SNHG6 in ESCC cell lines (TE1, Yes-2, Eca9706 and Kyse150). Then, TE1 cell line which harbored highest expression of SNHG6 was used in following experiments. siRNAs were used to knock down the expression of SNHG6. Clone formation, wound-healing and transwell assay were used to detect the abilities of proliferation, migration andinvasionofTE1cells,respectively.Westernblottingwasusedtodetecttheexpressions of MMP-2, MMP-9andZEB1 protein before and after knockdownofSNHG6inTE1cells.Results:SNHG6washighlyexpressedinESCC tissues, compared to para-carcinoma tissues (P<0.01). The expression of SNHG6 was significantly decreased after transfection of SNHG6siRNA (all P<0.01). The abilities of proliferation, migration and invasion of TE1 cells in si-SNHG6-1 and si-SNHG6-2 group were significantly lower than those in the control group (all P<0.01). The expressions of ZEB1, MMP-2and MMP-9 in si-SNHG6-1 and si-SNHG6-2 group were significantly lower than those in the control group (all P<0.05). Conclusion: SNHG6 is highly expressed in ESCC tissues and promotes the malignant biological behavior of ESCC cells. Its mechanism of promoting the occurrence and development of ESCC may be related to the upregulation of ZEB1 expression.

To investigate the role of long chain non-coding RNA00707 (lncRNA00707) and micro RNA-613 (miR-613) in regulating the proliferation and metastasis of gastric cancer cells and its underlying mechanisms. Methods: Eighty-nine pairs of primary gastric cancer tissues and corresponding prar-cancerous tissues were collected from the Department of Surgical Oncology, Qinghai Provincial People's Hospital during January 2014 and June 2018 for this study. The expressions of lncRNA00707 and miR-613 in gastric cancer tissues and cells were detected by qPCR. The lncRNA00707 low expression and over-expression models of MGC-803 and SGC-7901 cells were established; The proliferation of gastric cancer cells was monitored by CCK-8 assay, and Transwell assay was performed to determine the migration and invasion of gastric cancer cells. Dual luciferase gene reporter assay was adopted to validate the relationship between lncRNA 00707 and miR-613. Results: Compared with para-cancerous tissues and normal cell line GES-1, the expression of lncRNA 00707 was significantly up-regulated in cancer tissues and cell lines, and the expression of lncRNA00707 was positively correlated with WHO stage (all P<0.05). Down-regulation of lncRNA 00707 significantly inhibited the proliferation and migration of SGC-7901 cells, while overexpression of lncRNA00707 exerted the opposite effect (all P<0.05). Compared with negative control group, lncRNA00707 over-expression significantly reduced the luciferase activity of miR-613; in the contrary, the luciferase activity of miR-163 was significantly increased in MGC-803 and SGC-7901 cells with lncRNA 00707 knockdown (all P<0.01). Conclusion: lncRNA 00707 facilitates the proliferation, migration and invasion of gastric cancer cells by inhibiting the function of miR-613, which exerts a protumorigenic effect in gastric cancer.

[Abstract] Objective: To investigate the effect of apatinib (APA) combined with cisplatin (DDP) on the proliferation, invasion and migration capacity of gastric carcinoma (GC) cells and its molecular mechanism. Methods: Cancer and para-cancerous tissue samples resected from 50 GC patients, who were surgically treated in Wuwei People's Hospital from January 2016 to June 2019, were collected for this study; in addition, GC cell lines MGC803 and SGC7901 were also collected. qPCR was used to detect the HMGA2 expression in tissues and mRNA expressions of molecules related to cell proliferation, migration and invasion in GC cell lines. MGC803 and SGC7901 cells were transfected with pcHMGA2 by liposome transfection technology. After treatment with DDP and APA at different concentrations, the cells were divided into NC, pcHMGA2, pcHMGA2+DDP and pcHMGA2+DDP+APA groups. Protein expression of HMGA2 in GC cells was detected by Western blotting, and proliferation, migration and invasion of the cells were detected by MTT and Transwell assay, respectively. Results: The mRNA expression of HMGA2 in GC tissues was higher than that in para-cancerous tissues (P<0.05), and the survival rate of GC patients in the high expression group was significantly reduced (P<0.01). DDP significantly inhibited the proliferation, invasion and migration of MGC803 and SGC7901 cells (all P<0.01); the proliferation, invasion and migration of MGC803 and SGC7901 cells in DDP+APA group significantly decreased (all P<0.01) as compared with DDP group; APA significantly enhanced the inhibitory effect of DDP on HMGA2 expression in GC cells (P<0.01); APA enhanced the anticancer activity of DDP against GC by down-regulating HMGA2 expression. Conclusion: APA promotes the anticancer activity of DDP against GC, and its molecular mechanism is the promotion of the inhibitory effect of DDP on HMGA2 expression.

[摘 要] 目的：探讨LINC01503在上皮性卵巢癌（EOC）中的表达水平和生物学功能及其可能的作用机制。方法：收集2015年5月至2016年5月间在河北医科大学第四医院妇瘤科手术切除并经病理学确诊的85例EOC患者的肿瘤组织和输卵管组织。常规培养人EOC细胞A2780、SKOV3、OVCAR3和OV90及正常人卵巢上皮细胞IOSE80，将si-LINC01503、si-NC及miR-342-3p mimic、miR mimic NC分别转染至SKOV3和A2780细胞，分别作为si-LINC01503组、si-NC组、miR-342-3p mimic组和miR mimic NC组。qPCR法检测EOC组织和细胞中LINC01503的表达水平，Kaplan-Meier法分析LINC01503表达水平与患者生存的关系。双荧光素酶报告基因实验验证LINC01503/miR-342-3p/IGF2R轴相关分子间的靶向关系。平板克隆、划痕愈合和Transwell实验分别检测敲低LINC01503及转染miR-342-3p mimic对A2780和SKOV3细胞增殖、迁移和侵袭能力的影响。WB法检测EOC细胞中LINC01503/miR-342-3p通路对IGF2R蛋白表达的影响。构建A2780细胞裸鼠移植瘤模型，观察敲低LINC01503对移植瘤生长的影响。结果：EOC组织和细胞中LINC01503表达水平分别显著高于输卵管组织和IOSE80细胞（均P<0.01），LINC01503高表达组患者术后PFS和OS均显著短于LINC01503低表达组患者（均P<0.01）。敲低LINC01503、转染miR-342-3p mimic均可抑制EOC细胞的增殖、迁移和侵袭能力（均P<0.01）。敲低LINC01503可下调IGF2R的表达（P<0.01），这一现象可通过转染miR-342-3p inhibitor挽救。敲低LINC01503可抑制A2780细胞裸鼠移植瘤的生长（P<0.01）。结论：在EOC组织和细胞中呈高表达的LINC01503与患者的不良预后密切相关，LINC01503可能通过吸附miR-342-3p影响IGF2R表达进而促进EOC的进展。

[摘 要] 目的：探讨紫甘薯花色苷（purple sweet potato anthocyanin, PSPA）是否通过circ_0003998/miR-145轴调控乳腺癌MDA-MB-231细胞的增殖、迁移和侵袭。方法：选用乳腺癌MDA-MB-231细胞，将其分为对照组，200、400和800 μg/ml PSPA组，pcDNA组、pcDNA-circ_0003998组、si-NC组、si-circ_0003998组、si-circ_0003998+anti-miR-145组、PSPA+pcDNA组、PSPA+pcDNA-circ_0003998组和PSPA+anti-miR-145组。用qPCR法检测细胞中circ_0003998和miR-145的表达，CCK-8法、Transwell小室法分别检测转染前后细胞的增殖、迁移和侵袭能力，WB法检测细胞中Ki-67、MMP-2和MMP-9蛋白的表达。用双荧光素酶报告基因实验验证circ_0003998与miR-145的靶向关系。结果：与对照组比较，各剂量PSPA组MDA-MB-231细胞的增殖抑制率、miR-145表达水平均显著升高（均P<0.01），Ki-67、MMP-2、MMP-9蛋白和circ_0003998的表达水平、细胞迁移和侵袭细胞数均显著降低（均P<0.01），并呈现浓度依赖性。circ_0003998可以靶向负调控miR-145的表达。敲减circ_0003998后，MDA-MB-231细胞的增殖抑制率、miR-145表达水平显著升高，Ki-67、MMP-2和MMP-9蛋白表达水平、细胞迁移和侵袭细胞数均显著减少（均P<0.01）。共转染si-circ_0003998和anti-miR-145则可逆转敲减circ_0003998表达对MDA-MB-231细胞增殖、迁移和侵袭的抑制作用，过表达circ_0003998或抑制miR-145表达可逆转PSPA对MDA-MB-231细胞增殖、迁移和侵袭的抑制作用。结论：PSPA通过circ_0003998/miR-145轴抑制乳腺癌MDA-MB-231细胞的增殖、迁移和侵袭。

<b>Objective:b> To study the characteristics of social relations and relative factors among MSM in Guangzhou. <b>Methods:b> Data was collected through a cross-sectional study in Guangzhou from November 2016 to May 2017. Sample size was estimated and participants were recruited from the voluntary counseling and testing services (VCT) which were set for MSM population, by nongovernmental organizations (NGOs) and the Centers for Disease Control and Prevention (CDC). Social ties and demographic characteristics of the respondents and their sexual partners were analyzed through both Chi square test and generalized estimating equations (GEE). <b>Results:b> A total of 1 073 MSM, together with their nominated 4 301 partners were successfully recruited and involved in this study. Age (OR=1.2, P=0.01) and non-internet based intercourse (OR=1.65, P<0.01) were easy to form close relation with strong ties. Compared with MSM traditional venues (chess and cards room, tea room bathhouse, club), general public venue (bars, KTV, parks, shopping malls, schools, restaurants) (OR=1.46-3.12, P<0.01) showed close relation with strong ties. Our finding showed that MSM at the age of 18-25 preferred to build weak ties with the older MSM, while the 26-30-year-olds and 31-40-year-olds prefer to establish weak ties with younger partners but the 41-50-year-olds preferred to develop weak ties with one that were ten years younger. <b>Conclusions:b> Clusters were noticed in the MSM populations when grouping and making friends with ones at different age. Characteristics regarding the relationship between sexual partners in choosing venues and ways of dating were different. Targeted intervention programs need to be explored innovatively.
Coitus ; Cross-Sectional Studies ; Homosexuality, Male/psychology* ; Humans ; Interpersonal Relations ; Male ; Middle Aged ; Recreation ; Risk-Taking ; Schools ; Sexual Behavior ; Sexual Partners ; Social Behavior ; Surveys and Questionnaires

<b>Objective:b> To explore the reasons and factors associated with new psychoactive substances abuse among patients with access to methadone maintenance treatment (MMT). <b>Methods:b> A well-developed questionnaire and urine tests were used to collect information about demographic characteristics, condition of MMT and drug abuse, family and social support of MMT clients. A 1∶1 matched case-control study was conducted, and conditional logistic regression model was used to identify factors associated with new psychoactive substances abuse. <b>Results:b> A total of 212 (106 pairs) clients receiving MMT were recruited, and most of them were males (78.3%, 166/212), married or cohabitant (48.6%, 103/212) and unemployed (63.2%, 134/212). The average age of the clients was (45.1±7.2) years. The main types of abused new psychoactive substances were benzodiazepine (62.3%, 66/106) and methamphetamine (39.6%, 42/106). The proportion of abusing multi new psychoactive substances was 8.5% (9/106). Results from multivariate conditional logistic regression analysis indicated that using opioid drug during the past 6 months of MMT treatment might increase the risk of abusing new psychoactive substances (OR=3.25, 95%CI: 1.35-7.79), benzodiazepine (OR=3.25, 95%CI: 1.11- 9.47) and methamphetamine (OR=13.31, 95%CI: 1.12-158.01). Moreover, MMT for more than9 years reduced the risk of abuse of new psychoactive substances (OR=0.03, 95%CI: 0.01-0.21), benzodiazepine (OR=0.02, 95%CI: 0.00-0.36) and methamphetamine (OR=0.02, 95%CI: 0.00-0.69). <b>Conclusion:b> Less new psychoactive substances abuse might be associated with longer duration of MMT treatment. And inappropriate support from family and friends might increase the risk of abusing new psychoactive substances in MMT clients, especially in clients who used opioid.
Adult ; Case-Control Studies ; China/epidemiology* ; Drug Users/statistics & numerical data* ; Humans ; Logistic Models ; Male ; Methadone/therapeutic use* ; Methamphetamine ; Middle Aged ; Opiate Substitution Treatment ; Prevalence ; Psychotropic Drugs/adverse effects* ; Substance Abuse Detection/statistics & numerical data* ; Substance Abuse Treatment Centers ; Substance-Related Disorders/epidemiology* ; Surveys and Questionnaires

Humans ; Erdheim-Chester Disease/diagnostic imaging* ; Histiocytosis, Langerhans-Cell/surgery* ; Tomography, X-Ray Computed