ABSTRACT
Abstract Objectives Metastasis is one of the biggest challenges in the management of Esophageal Squamous Cell Carcinoma (ESCC), of which molecular mechanisms remain elusive. The present study aimed to explore the roles and underlying mechanisms of Transmembrane protein 26 (TMEM26) in ESCC. Method TMEM26 expressions in tumorous and adjacent tissues from patients with ESCC and in normal esophageal epithelial and ESCC cell lines were detected by immunostaining and western blotting, respectively. The Epithelial-Mesenchymal Transition (EMT), a critical process during metastasis, was investigated by wound healing and Transwell assays, and EMT-related proteins were examined after the TMEM26 alteration in ESCC cell lines. NF-κB signaling activation and Tight Junction (TJ) protein expression were analyzed by western blotting and immunofluorescence, respectively. In vivo verification was performed on the liver metastatic murine model. Results Compared with non-cancerous esophageal tissues and cells, the TMEM26 expression level was higher in ESCC samples and cell lines, where the plasma membrane localization of TMEM26 was observed. The EMT-related processes of ESCC cells were suppressed by RNAi depletion of TMEM26 but aggravated by TMEM26 overexpression. Mechanistically, TMEM26 promoted NF-κB signaling to accelerate EMT in ESCC cells. The plasma membrane presentation and assembly of TJ proteins were impaired by TMEM26. Conclusion Overall, TMEM26 acts as a critical determinant for EMT in ESCC cells by disrupting TJ formation and promoting NF-κB signaling, which may be a potential therapeutic target for treating metastatic ESCC.
ABSTRACT
Objective@#To understand and explore the fear-related emotional disorder and its influencing factors among college students during the prevalence of coronavirus disease 2019 （COVID-19）, in order to provide reference for the further health education and psychological intervention. @*Methods@#A self-designed questionnaire for general data and Psychological Questionnaires for Emergent Events of Public Health （PQEEPH） were typed in www.wjx.cn and sent out to the students of four univerties in Xi'an by WeChat from February 7th to 9th,2020. The status and influencing factors of fear-related emotional disorder in response to COVID-19 were analyzed. @*Results@#Totally 1 546 valid questionnaire were collected. The average age of the students was （20.24±1.60）years old. There were 761 males（49.22%）and 785（50.78%）females;499 medical students （32.27%）and 1 047 non-medical students（67.72%）. The average score of fear dimension was 0.90±0.59,which was the highest in PQEEPH. Moreover, 280 students had fear-related emotional deviance,accounting for 18.11%,and 57 students had fear-related emotional disorder,accounting for 3.69%. The rate of fear-related emotional disorder was significantly higher in non-medical students（4.58%）than in medical students（1.80%,P<0.05）. The rate of fear-related emotional disorder was significantly higher in the students who considered themselves close to COVID-19（4.22%）and at risk of COVID-19（5.45%） than in the students who did not（1.94% and 0.98%,both P<0.05）. @*Conclusions@#Totally 3.69% of the students from universities in Xi'an suffer from fear-related emotional disorder in response to COVID-19. The students who do not major in medicine are prone to developing fear-related emotional disorder.
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Objective@#To explore the psychological responses and related factors of college students in Shaan’xi during the outbreak of COVID-19, in order to provide reference for the psychological intervention for college students.@*Methods@#A self-designed general data questionnaire and Psychological Questionnaires for Emergent Events of Public Health(PQEEPH) were sent out to students in public university aged 18 to 28 years by Wechat APP from February 7th to 9th, 2020. Univariate and Logistic analysis were used to analyze the influencing factors associated with NCP.@*Results@#The scores of the five factors on the PQEEPH scale were (0.29±0.48) for depression, (0.27±0.46) for neurasthenia, (0.92±0.60) for fear, (0.15±0.34) for obsessive-anxiety, and (0.26±0.44) for hypochondria，The score of fear factors were the highest. And 15.4% had depressive emotional deviation, accounting for the highest proportion of emotional deviation, and the proportion of compulsive anxiety emotional disorder was highest, which accounting for 6.4%. Logistic regression analysis showed that the higher grades were risk factors for depression (OR=1.61, 95%CI=1.05-2.47), obsessive anxiety (OR=1.56, 95%CI=1.05-2.31) and hypochondria (OR=2.01, 95%CI=1.16-3.47) disorders, Non-medical specialties is risk factor for fear disorders (OR=2.16, 95%CI=1.18-3.95)，not believing oneself to be in danger in the face of the epidemic was a protective factor for five types of mood disorders (OR=0.17-0.51), and residence in towns and villages was a protective factor for neurasticity disorders (OR=0.58, 95%CI=0.38-0.87), the gender of female was the protective factor of hypochondria emotional disorder (OR=0.34, 95%CI=0.19-0.62)(P<0.05).@*Conclusion@#During outbreak of COVID-19, psychological intervention counselling and health education of college students should be strengthened. Moreover, psychological problems need be screened in time for intervention, so as to reduce panic and other adverse psychological conditions of students.
ABSTRACT
Swainsonine, a natural indolizidine alkaloid, has been reported to have antitumour effects, and can induce apoptosis in human gastric and lung cancer cells. In the present study, we evaluated the antitumour effects of swainsonine on several oesophageal squamous cell carcinoma cells and investigated relative molecular mechanisms. Swainsonine treatment inhibited the growth of Eca-109, TE-1 and TE-10 cells in a concentration-dependent manner as measured by MTT assay. Morphological observation, DNA laddering detection and flow cytometry analysis demonstrated that swainsonine treatment induced Eca-109 cell apoptosis in vitro. Further results showed that swainsonine treatment up-regulated Bax, downregulated Bcl-2 expression, triggered Bax translocation to mitochondria, destructed mitochondria integrity and activated mitochondria-mediated apoptotic pathway, followed by the release of cytochrome c, which in turn activated caspase-9 and caspase-3, promoted the cleavage of PARP, resulting in Eca-109 cell apoptosis. Moreover, swainsonine treatment inhibited Bcl-2 expression, promoted Bax translocation, cytochrome c release and caspase-3 activation in xenograft tumour cells, resulting in a significant decrease of tumour volume and tumour weight in the swainsoninetreated xenograft mice groups compared with that in the control group. Taken together, this study demonstrated that swainsonine inhibited Eca-109 cells growth through activation of mitochondria-mediated caspase-dependent pathway.