Sinonasal malignancies (SNMs) are rare, heterogeneous, and aggressive. High-quality evidence to guide management is limited, and the prognostic value of multidisciplinary team (MDT) management remains incompletely characterized. This study aims at evaluating the association of MDT management with survival outcomes and treatment selection among patients with SNMs. Retrospective cohort study including 304 consecutive patients with histologically confirmed SNMs treated at the First Affiliated Hospital of Sun Yat-sen University between September 2017 and December 2023. Patients were classified according to whether their cases underwent a formal MDT review process before the definitive treatment plan was initiated. The primary outcome was overall survival (OS). Baseline differences were addressed using stabilized inverse probability of treatment weighting (IPTW). Survival was analyzed with Kaplan-Meier estimates and weighted Cox proportional hazards models. Treatment patterns were compared using weighted logistic regression. Secondary outcomes included length of hospital stay and hospitalization costs. Of 304 included patients, 106 (34.9

Background: Porphyromonas gingivalis lipopolysaccharide (P.g-LPS), a key virulence factor in periodontitis, contributes to systemic vascular diseases, notably atherosclerosis. MicroRNA-21 (miR-21), a critical post-transcriptional regulator, influences inflammation and vascular pathology, but its role in endothelial responses to P.g-LPS remains unclear. Methods: Gingival biopsies from eight patients with periodontitis and eight healthy controls were analyzed using immunofluorescence co-labeling for Cluster of Differentiation 31 (CD31) with TUNEL or Interleukin-6 (IL-6) to assess endothelial apoptosis and inflammation. MiR-21 levels were quantified using quantitative Reverse Transcription Polymerase Chain Reaction (RT-PCR). Human umbilical vein endothelial cells (HUVECs) were treated with P.g-LPS and transfected with miR-21 mimics or inhibitors. Apoptosis, proliferation, and migration were evaluated by flow cytometry, Cell Counting Kit-8 (CCK-8) assay, and wound healing analysis, respectively. Western blotting and Enzyme-Linked Immunosorbent Assay(ELISA) measured inflammatory and apoptotic markers. Luciferase reporter assays confirmed that PDCD4 was a direct target of miR-21, and the effects of Programmed Cell Death 4(PDCD4) knockdown on Nuclear Factor kappa B (NF-κB)/Inducible Nitric Oxide Synthase (iNOS)/Nitric Oxide (NO) signaling were examined. Results: Endothelial cells from patients with periodontitis exhibited increased apoptosis and inflammation. P.g-LPS significantly reduced miR-21 expression in HUVECs. MiR-21 inhibition exacerbated apoptosis and inflammatory mediator expression, while suppressing proliferation and migration.MiR-21 overexpression mitigated these effects. PDCD4 was validated as a direct miR-21 target. Suppression of miR-21 enhanced NF-κB/iNOS/NO activation, and PDCD4 knockdown attenuated this pathway, indicating a regulatory mechanism. Conclusion: MiR-21 acts as a protective regulator against P.g-LPS-induced endothelial injury by targeting PDCD4 and modulating the NF-κB/iNOS/NO pathway, thereby reducing inflammation and apoptosis. These findings indicate that miR-21 is a potential therapeutic target for vascular complications associated with chronic inflammatory diseases like periodontitis.

Background: Recent researches have demonstrate that cuproptosis, a copper -dependent cell death mechanism, is related to tumorigenesis, progression, clinical prognosis, tumor microenvironment, and drug sensitivity. Nevertheless, the function and impact of cuproptosis in cholangiocarcinoma (CCA), remain elusive. Methods: Utilizing data obtained from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA-CHOL) datasets, we conducted subgroup typing of CCA according to cuproptosis-related genes (CRGs) and explored functional differences and prognostic value between groups. A CRG score was established considering clinical prognosis and gene expression. Furthermore, differences in the immune microenvironment, response to immunotherapy, metabolic patterns, and cancer progression characteristics between high- and low -risk groups were examined on the basis of these scores. In vitro experiments validated the function of the key gene glycine cleavage system protein H (GCSH) in cellular and tissues, respectively. Results: Prognostic models established on the basis of subgroup genetic differences achieved satisfactory results in validation. Metabolic -related gene expression levels and tumor microenvironment distribution were significantly different between the high and low CRG groups. GCSH was revealed as the singular prognostic CRG in CCA (HR =6.04; 95% CI: 1.15-31.80). Moreover, inhibition of the cupcoptosis key gene GCSH attenuated the malignant ability of CCA cell lines in vitro, including cell proliferation, migration and invasion, and this function of GCSH may be achieved via JAK-STAT signaling in CCA. Conclusion: The CRG scoring system accurately predicts prognosis and opens up new possibilities for cuproptosis-related therapy for CCA. The cuproptosis key gene GCSH has been preliminarily confirmed as a reliable therapeutic target or prognostic marker for CCA patients.

BACKGROUND:Activated regulatory T cells (aTregs) play a vital role in promoting a tumor immunosuppressive microenvironment in laryngeal squamous cell carcinoma (LSCC). However, the regulatory factors that induce the generation of aTregs are not clear. Herein, we investigated the effect of amphiregulin (AREG) on the production of aTregs in the tumor microenvironment of LSCC. METHODS:Immunohistochemical (IHC) analysis was conducted to examine the expression of AREG and FOXP3, and their association with clinical parameters and patient outcomes was demonstrated. The expression level of EGFRs in three functional subsets of Tregs was assessed, and the induction of CD4+ T cells into aTregs in the presence or absence of AREG or Gefitinib was analyzed using flow cytometry. RESULTS:Our results showed a higher expression level of AREG was significantly related to advanced clinical stage and worse survival, particularly with increased infiltration of Tregs in LSCC tumor tissue. The in vitro study showed that AREG significantly promoted the differentiation of aTregs, and enhanced the inhibitory effect of Tregs on T cell proliferation, which could be reversed by epidermal growth factor receptor (EGFR) inhibitors. In addition, we found that EGFR was highly expressed in aTregs, but not in other subsets of Tregs. It is suggested that AREG might induce aTregs, and enhance the immunosuppressive function of Tregs via the AREG/EGFR signal pathway. CONCLUSIONS:Collectively, this study revealed the role and mechanism of AREG in negative immune regulation, and targeting AREG might be a novel immunotherapy for LSCC.

Objective:To establish donor liver quality related risk factors for the loss of function of transplanted liver.Methods:The data of donors and recipients of liver transplantation at the Organ Donation and Transplantation Center of the First Affiliated Hospital of Sun Yat-sen University from Nov 2011 to Dec 2018 were analyzed retrospectively. Propensity score matching (PSM) was performed to evaluate and screen the data of donors and recipients, in order to balance the covariates.Results:Of the organ donation, there were 70 males and 20 females , aging (40.6±16.3) years. Of the liver transplantation recipients, there were 70 males and 20 females , aging (41.8±20.3) years. Liver dysfunction after transplantation was significantly correlated with the following variables: the donor's CPR time( t=0.429, P=0.000), 15-minute retention rate of indocyanine green ( χ2=67.151, P=0.000), liver function grading ( χ2=54.154, P=0.000), bullae fatty liver grading ( χ2=8.120, P=0.017), vesicular fatty liver grading ( χ2=16.000, P=0.001), ICU stay time ( χ2=14.900, P=0.001)and serum creatinine level ( χ2=44.685, P=0.000). The donor scoring system was established in our studying. For the 90 organ donation cases, the donated liver quality were classified into four levels,which were of good correspondence to the prognosis of the recipients. Conclusion:This donor scoring system and grading standards established by analyzing the high-risk factors of liver dysfunction after transplantation helps evaluate the quality of donor liver in China.

Background: Circular RNAs (CircRNAs) and their associations with human disease have been widely studied. However, the roles of circRNAs in gallstone disease (GD) remain uncertain.Methods: We recruited 1134 gallstone first formation patients, 2068 gallstone free controls, 158 gallstone second formation patients and 644 recovered patients. The expression level 12 candidate circRNAs from patients’ serum samples was determined by quantitative polymerase chain reaction. We then explored the potential of using candidate circRNAs as independent genetic risk factors and novel diagnostic biomarkers for gallstone first and second formation.Findings: Among 12 candidate circRNAs, circHIPK3 and hsa_circ_0014243 were significantly increased in GD patients (All P>0.05). After controlling common risk factors, circHIPK3 (phase 1: OR 1.33; 95% CI 1.10 ~ 1.60) (phase 2: OR 1.47; 95% CI 0.97 ~ 2.23) and hsa_circ_0014243 (phase 1: OR 1.29; 95% CI 1.06 ~ 1.57) (phase 2: OR 1.46; 95% CI 0.98 ~ 2.17) were identified as independent risk factors for GD. GD patients with increased expression of circHIPK3 and high triglyceride showed the highest OR. In phase 1, the area under the receiver operating characteristic curve (AUC) for circHIPK3 and hsa_circ_0014243 were 0.81 and 0.73, respectively. Similarly, the AUC in phase 2 were 0.79 and 0.66, respectively.Interpretation: circHIPK3 and hsa_circ_0014243 may be independent genetic risk factors and novel diagnostic biomarkers for gallstone first and second formation.Funding Information: The Committee of National Natural Science Foundation.Declaration of Interests: No potential conflict of interest relevant to this article was reported. Ethics Approval Statement: All protocols in this study were approved by the ethics committee of Dong Guan Nan Cheng Hospital and The First Affiliated Hospital, Sun Yat-sen University. Informed consent was provided to all participants, and the study protocol conformed to the ethical guidelines of the Declaration of Helsinki (1975).

BACKGROUND:Drug resistance is a major obstacle to treating cancers because it desensitizes cancer cells to chemotherapy. Recently, attention has been focused on changes in the tumor immune landscape after the acquisition of drug resistance. Programmed death-ligand-1 (PD-L1) is an immune suppressor that inhibits T cell-based immunity. Evidence has shown that acquired chemoresistance is associated with increased PD-L1 expression in cancer cells. However, the underlying mechanism is still largely unknown.METHODS:PD-L1 expression in three drug-resistant A549/CDDP, MCF7/ADR and HepG2/ADR cell lines was detected by qRT-PCR, western blotting and flow cytometry, and a T cell proliferation assay was performed to test its functional significance. Then, the potential roles of JNK/c-Jun, histone H3 acetylation, histone deacetylase 3 (HDAC3) and the E3 ligase COP1 in the PD-L1 increase were explored through ChIP assays and gain- and loss-of-function gene studies. Furthermore, murine xenograft tumor models were used to verify the role of JNK/c-Jun and HDAC3 in PD-L1 expression in A549/CDDP cells in vivo. Finally, the correlations of PD-L1, c-Jun and HDAC3 expression in clinical cisplatin-sensitive and cisplatin-resistant non-small cell lung cancer (NSCLC) tissues were analyzed by immunohistochemistry and Pearson's correlation coefficient.RESULTS:PD-L1 expression was significantly increased in A549/CDDP, MCF7/ADR and HepG2/ADR cells and was attributed mainly to enhanced JNK/c-Jun signaling activation. Mechanistically, decreased COP1 increased c-Jun accumulation, which subsequently inhibited HDAC3 expression and thereby enhanced histone H3 acetylation of the PD-L1 promoter. Furthermore, PD-L1 expression could be inhibited by JNK/c-Jun inhibition or HDAC3 overexpression in vivo, which could largely reverse inhibited CD3+ T cell proliferation in vitro. PD-L1 expression was significantly increased in the cisplatin-resistant clinical NSCLC samples and positively correlated with c-Jun expression but negatively correlated with HDAC3 expression.CONCLUSIONS:Enhanced histone H3 acetylation of the PD-L1 promoter via the COP1/c-Jun/HDAC3 axis was crucial for the PD-L1 increase in drug-resistant cancer cells. Our study reveals a novel regulatory network for the PD-L1 increase in drug-resistant cancer cells and that combined PD-L1-targeting strategies could improve T cell-based immunity in drug-resistant cancers.

目的 探讨替格瑞洛联合瑞舒伐他汀治疗冠心病的临床疗效及其对颈动脉粥样硬化的影响.方法 选取佛山市第一人民医院2018年4月—2019年3月收治的冠心病患者92例,采用随机数字表法分为对照组与观察组,各46例.对照组予以瑞舒伐他汀治疗,观察组在对照组基础上予以替格瑞洛治疗.2组均连续治疗3个疗程.比较2组临床疗效,治疗前后颈动脉斑块指标〔颈动脉内膜-中层厚度(IMT)及斑块厚度〕、心功能指标〔左心室射血分数(LVEF)、左心室舒张末期半径(LVEDD)〕、组织基质金属蛋白酶抑制物1(TIMP-1)水平,并观察2组不良心血管事件(MACE)发生情况.结果 观察组临床疗效优于对照组(P<0.05).治疗前2组IMT、斑块厚度比较,差异无统计学意义(P>0.05);治疗后观察组IMT、斑块厚度薄于对照组(P<0.05).治疗前2组TIMP-1水平、LVEF、LVEDD比较,差异无统计学意义(P>0.05);治疗后观察组TIMP-1水平低于对照组,LVEF高于对照组,LVEDD小于对照组(P<0.05).观察组MACE发生率低于对照组(P<0.05).结论 替格瑞洛联合瑞舒伐他汀治疗冠心病的临床疗效确切,可延缓颈动脉粥样硬化发展,降低TIMP-1水平,改善心功能,减少MACE发生治疗结果.

目的 观察安全管理在西药房高警示药品管理中的应用价值.方法 选择佛山市第一人民医院(中山大学附属佛山医院)西药房2018年1-12月收录的使用高警示药品的患者240例,采用随机数字表法分成研究组和对照组,每组120例.对照组采用常规模式管理,研究组采用安全管理模式管理.比较2组药品使用错误次数、患者对高警示药品管理和服务工作的满意度评分及所致用药不良事件发生率.结果 研究组药品使用错误次数显著少于对照组,患者对药品管理和服务工作的满意度评分显著高于对照组(P<0.01);研究组药品所致用药不良事件发生率显著低于对照组(χ2=49.645,P=0.000).结论 在西药房高警示药品管理中应用安全管理,不仅能有效减少药品使用错误次数,还能降低药品所致用药不良事件发生率,提高其对高警示药品管理和服务工作的满意度,从而为患者提供安全、有效的用药服务.

目的 探究妊娠期念珠菌性阴道炎患者采用凯妮汀药物的临床治疗效果.方法 选取我院2017年6月至2018年8月收治的68例妊娠期念珠菌性阴道炎患者作为研究对象,随机将患者分为对照组(n=34)和观察组(n=34),将制霉菌素应用于对照组临床,观察组采用凯妮汀治疗,对两组患者临床治疗效果进行比较.结果 两组患者临床治疗总有效率的比较,观察组高于对照组(P<0.05);且两组患者药物不良反应发生率的比较,观察组低于对照组(P<0.05).结论 对妊娠期念珠菌性阴道炎患者采用凯妮汀药物治疗能取得良好疗效,其有助于提高患者临床治疗效果,且该治疗方法的不良反应发生率较低,其值得推广使用.

目的 探讨氨氯地平阿托伐他汀钙片治疗高血压并冠心病的临床疗效及其安全性.方法 选取佛山市第一人民医院2017年9月—2018年9月收治的高血压并冠心病患者78例,采用随机数字表法分为参照组与试验组,各39例.参照组给予阿托伐他汀钙片治疗,试验组给予氨氯地平阿托伐他汀钙片治疗,两组均连续治疗3个月.比较两组治疗前后收缩压、舒张压、三酰甘油、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇,并比较两组临床疗效,观察两组不良反应发生情况.结果 治疗前两组收缩压、舒张压比较,差异无统计学意义(P>0.05);治疗后试验组收缩压、舒张压低于参照组(P<0.05).治疗前两组三酰甘油、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇比较,差异无统计学意义(P>0.05);治疗后试验组三酰甘油、总胆固醇、低密度脂蛋白胆固醇低于参照组,高密度脂蛋白胆固醇高于参照组(P<0.05).试验组总有效率高于参照组(P<0.05).两组不良反应发生率比较,差异无统计学意义(P>0.05).结论 氨氯地平阿托伐他汀钙片治疗高血压并冠心病的临床疗效确切,可调节其血压及血脂指标,且安全性较高.

目的 探讨沙丁胺醇联合沙美特罗替卡松粉吸入剂吸入治疗支气管哮喘急性发作的临床疗效.方法 选取佛山市第一人民医院2016年1月—2018年11月收治的支气管哮喘急性发作患者64例,按照抽签法分为对照组与试验组,各32例.对照组予以沙丁胺醇吸入治疗,试验组在对照组基础上联合沙美特罗替卡松粉吸入剂吸入治疗,两组均连续治疗1周.比较两组咳嗽、气促缓解时间及肠鸣音消失时间,临床疗效,治疗前后用力肺活量(FVC)、呼气流速峰值(PEF)、第1秒用力呼气容积(FEV1)、血清免疫球蛋白E、嗜酸粒细胞数目.结果 试验组咳嗽、气促缓解时间及肠鸣音消失时间短于对照组,临床疗效优于对照组(P<0.05).治疗前两组FVC、PEF、FEV1比较,差异无统计学意义(P>0.05);治疗后试验组FVC、PEF、FEV1高于对照组(P<0.05).治疗前两组血清免疫球蛋白E、嗜酸粒细胞数目比较,差异无统计学意义(P>0.05);治疗后试验组血清免疫球蛋白E、嗜酸粒细胞数目低于对照组(P<0.05).结论 沙丁胺醇联合沙美特罗替卡松粉吸入剂吸入治疗支气管哮喘急性发作的临床疗效确切,可改善患者肺功能,减轻炎性反应.

Objective To study the expression of MREll-RAD50-NBS1 complex in normal gallbladder tissues,simple cholecystitis,calculous cholecystitis and gallbladder carcinoma.Methods The expression of MRN complex in different gallbladder lesion tissues were detected by immunohistochemistry.Western blot,Methyl thiazolyl tetrazolium(MTT) assay and flow cytometry were used to detect the influence of apoptosis and proliferation induced by NBS1.Results The differences between the expression of MRE11,RAD50 and different gallbladder lesion tissues were not statistically significant (respectively x2 =2.724,1.697,all P ＞ 0.05).The expression of NBS1 in GBC tissues [15.3％ (9/59)] was prominently lower than that in the normal gallbladder tissues [84.7％ (50/59)],simple cholecystitis [87.8％ (36/41)],calculous cholecystitis [61.2％ (30/49)] (x2 =87.388,P ＜ 0.01).The Western blot results reveal that NBS1 can mediate apoptosis by up-regulate Bax and down-regulate Bcl-2.The MTT assay results showed that the relative absorbance of treatment and control group after 24,48,72 h were[(1.120 ± 0.006)vs.(1.350±0.009),(1.600±0.004)vs.(1.99±0.01),(1.83±0.01)vs.(2.260±0.003)(F=7.659,P ＜0.01).The apoptosis rate in treatment group(17.23％ ± 0.56％)was higher than that in the control group (4.13％ ± 0.67％) (t =9.133,P ＜ 0.01).Conclusion NBS1 is closely related to gallbladder carcinoma.NBS1 can inhibit the proliferation and promote apoptosis of GBC-SD cells.

目的:探讨顺尔宁联合信必可都保与单用信必可都保治疗支气管哮喘的应用效果.方法:选取2017年4月—2018年4月我院收治的支气管哮喘患者96例,按照随机对照原则分成对照组和观察组,各48例.对照组单用信必可都保治疗,观察组给予顺尔宁联合信必可都保治疗,比较两组肺功能、炎性因子、治疗效果.结果:与对照组相比,观察组PEFR、FEV1、FVC、治疗总有效率较高,TNF-α、IL-6、hs-CRP较低(P<0.05).结论:顺尔宁与信必可都保联合治疗支气管哮喘患者,可有效改善患者的肺功能,降低炎性因子水平,提高治疗效果,促进患者康复.

Objective Study on the mechanism of sliencing microRNA (miRNA,miR)-16 on chemoresistance in SMMC-7721.Methods The lentiviral vectors were used to construct stable cell lines.To determine whether constructed successfully,the expression of miR-16 was detected by real-time reverse transcription-polymerase chain reaction (RT-qPCR) and inhibitor of kappaB kinase beta (IKBKB),the target gene of miR-16,was detected by Western blotting.The sensitivity and resistance mechanism of the stable cell lines to paclitaxel were detected by Western blotting and thiazole blue (MTT).Results The expression of miR-16 in 7721-miR16 group was significantly higher than SMMC-7721 and 7721-mock groups (4.63 ± 1.32 vs.1.00 ± 0.30 vs.0.93 ± 0.37,P =0.000).The expression of IKBKB in 7721-shmiR16 was 25.73 times than the controls (P =0.000).The expression of multidrug resistance protein 1 (MDR1) in 7721-shmiR16 was increased and the half maximal inhibitory concentration (IC50) to paclitaxel was 4.903 μmol/L,10.64 times than the control group (0.461 μmol/L) (P =0.000).The results of western showed that silencing miR-16 induced resistance mainly through activating nuclear factor-kappaB (NF-κB) pathway.Conclusion Silencing miR-16 in SMMC-7721 significantly increases IKBKB expression leadind paclitaxel resistance.

Hepatocellular carcinoma (HCC) is a common malignant tumor usually resistant to chemotherapy. MicroRNAs play important roles in modulation of carcinogenesis and chemoresistance, which miR-16 has been reported to mediate chemoresistance in many types of cancers. However, the role of miR-16 in HCC remains unknown. The aim of this study was to investigate whether miR-16 is participated in chemoresistance in HCC and shed light on the underlying molecular mechanisms. The findings of the current study discover that miR-16 is down-regulated in HCC tissue and cell lines. The results demonstrate that the inhibition of miR-16 renders resistance to paclitaxel in vitro and in vivo by targeting IKBKB via NF-κB signaling pathway, suggesting that miR-16 may be a meaningful therapeutic potential to overcome drug resistance in HCC.

Objective To study the expressions of Nodal in normal gallbladder,and gallbladders with cholelithiasis,cholecystitis and carcinoma;and to study the impact of inhibiting or promoting Nodal expressions in gallbladder carcinoma on the Smad2/4 pathway and epithelial-mesenchymal transition.Methods Immunohistochemistry was used to detect the expressions and distributions of Nodal protein in 30 normal gallbladders,96 simple cholecystitis/calculous cholecystitis specimens and 42 gallbladder carcinoma specimens.The mRNA and protein expressions of Nodal in normal and malignant gallbladdcr mucosal epithelium cells and breast cancer cells were detected by RT-PCR,western blotting and wound healing tests.The impact of activating agents and inhibitors on the expression levels of Nodal and its signaling pathway Smad2/4 and EMT-related proteins were analyzed.Results Immunohistochemistry showed that the positive rates of Nodal in the gallbladder cancer group was significantly higher than that in the gallbladder stone group and the normal gallbladder group.The results were 83.3％ (35/42),44.8％ (43/96),6.7％ (2/30) respectively (P＜ 0.01).RT-PCR and Western blotting showed the expressions of Nodal in gallbladder carcinoma cells were higher than normal gallbladder cells (P＜0.05).After using rhNodal to up regulate the Nodal expression,the Smad2 protein phosphorylation was promoted and the EMT associated proteins were up-regulated.After using the inhibitor SB431542 to suppress the Nodal expression,the Smad2 protein phosphorylation decreased and the EMT associated proteins were down-regulated.Conclusions The expression of Nodal was closely related to cell proliferation and metastasis in gallbladder carcinoma.Tumor progression was promoted via the smad2/4 pathway through epithelial-mesenchymal transition.

Objective To investigate the expressions of Yes-associated protein-1 (YAP1) in gallbladder mucosal epithelium of normal persons,in patients with simple/calculous cholecystitis,and in patients with gallbladder carcinoma;and to study the mechanism of YAP1 in gallbladder carcinoma development.Methods Immunohistochemistry was used to detect the expression and distribution of YAP1 protein in 50 persons with normal gallbladder,101 patients with simple cholecystitis/calculous cholecystitis and 100 patients with gallbladder carcinoma.RT-PCR and western-blot were used to detect the mRNA and protein levels of YAP1 in normal and malignant gallbladder mucosal epithelium cells.siRNA was used to shut down the expression of YAP1 in SGC996 cells.MTT was used to test cell vitality.Flow cytometry was used to measure cell cycle.Results Immunohistochemistry revealed the expression rates of YAP1 in the gallbladder carcinoma group,the cholecystitis/gallstone group and the control group to be 87.0％ (87/100),56.4％ (57/101) and 5.0％ (1/20),respectively (P ＜ 0.01).The YAP1 protein levels were higher in gallbladder carcinoma tissues and cells when compared to normal tissues and cells.RT-PCR showed the mRNA levels of gallbladder carcinoma cells to be 12.5 ± 1.2 times of normal gallbladder mucosal epithelial cells (P ＜ 0.05).After using siRNA to shut down the YAP1 expression,EMT associated proteins were down-regulated,cell vitality was decreased,and cell cycle was arrested in the S-phase.Conclusions YAP1 is closely related to cell proliferation and metastasis of gallbladder carcinoma.It may promote tumor progression through epithelial-mesenchymal transition.transition;Tumor progress

Gallbladder carcinoma (GBC) is the most common malignancy of the bile duct and patients with GBC have extremely poor prognoses. Increasing evidence indicates that long non-coding RNAs (lncRNAs) regulate diverse cellular processes, including cell growth, differentiation, apoptosis, and cancer progression. However, the function of lncRNAs in the progression of GBC remains largely unknown. Here, we reported that HOXA cluster antisense RNA2 (HOXA-AS2) was upregulated in GBC. In vitro experiments revealed that HOXA-AS2 knockdown significantly inhibited GBC cells proliferation by causing G1 arrest and promoting apoptosis, whereas HOXA-AS2 overexpression promoted cell growth. Further functional assays indicated that HOXA-AS2 overexpression significantly promoted GBC cell migration and invasion by promoting EMT. Taken together, our study demonstrates that HOXA-AS2 could act as a functional oncogene in GBC, as well as a potential therapeutic target to inhibit GBC metastasis.

Objectives To acquire the hospitalization situation operation inpatients with primary gallbladder carcinoma in a hospital, and provide evidence for improving feelings of patients and strengthen hospital management. Methods The clinical materials of 291 cases of operation inpatients with primary gallbladder carcinoma in the hospital during the past ten years from 2005 to 2014 with the application of retrospective survey method, the data of patients including gender, age, pathological type, treatment, results, hospitalized days, cost and so on were analyzed. Results Male cases were 144(49.5%), female cases were 147(50.5%), the ratio of male compared with female was 0.97:1, the youngest age was 27 years old, the oldest age was 87 years old, and average age was (57.81±18.53) years , including 69 cases were smaller than 50 years old, 89 cases were from 50 years old to 60 years old, 79 cases were from 60 years old to 70 years old, 49 cases were from 70 years to 80 years old, 5 cases were bigger than 80 years old. The main approach of primary gallbladder carcinoma was radical resection. The cure rate of surgery was 36.77%during the 10 years. Period before and after operation were respectively (8.47±5.17)days and(16.63±8.26) days, and average hospital stay was (25.38±11.36)days, and average hospitalization cost was RMB(58276.23±5553.36)yuan, proportion of drug fees up to (41.59±9.98)%. Conclusions The elderly should pay attention to the occurrence of primary gallbladder carcinoma. The curative effect on primary gallbladder cancer is improving year by year, and the increase of hospitalization expenses is reasonable.