Cervical cancer is a common tumor of the reproductive system; however, to the best of the authors' knowledge, the regulation and underlying mechanism of p53 apoptosis-stimulating protein 2 (ASPP2) in cervical cancer has yet to be elucidated. Therefore, the present study aimed to explore the role of ASPP2 in cervical cancer. Tumor tissues were collected for the detection of ASPP2 expression. Experiments wherein ASPP2 was overexpressed were designed to upregulate the expression of ASPP2. The levels of autophagy were subsequently assessed by examining LC3B level via immunofluorescence. Cell Counting Kit-8 assay was then performed to estimate the level of cell proliferation. The cell proliferation level was also measured by EdU staining, and TUNEL assay was used to detect the level of apoptosis. The expression levels of ASPP2, Beclin1 and associated proteins were detected using reverse transcription-quantitative PCR and western blotting analyses. ASPP2 was observed to be markedly reduced in patients with cervical cancer and in cervical cancer cell lines. Overexpression of ASPP2 was found to suppress the expression of Beclin1, and autophagy was also inhibited in cervical cancer cells. Overexpression of ASPP2 also inhibited cell proliferation and promoted apoptosis of cervical cancer cells via the inhibition of autophagy. Additionally, overexpression of ASPP2 was shown to enhance the TNF-related apoptosis-inducing ligand-induced apoptosis of cervical cancer cells via inhibiting autophagy. Taken together, the results of the present study have shown that ASPP2 exerted antitumor effect in cervical cancer by inhibiting cell proliferation and promoting apoptosis partly through inhibiting autophagy. These findings may be useful for the provision of potential targets for cervical cancer therapy.

People's lives were significantly impacted when China underwent a self-quarantine period, spanning multiple weeks to months, due to COVID-19. The impacts of this quarantine included disruption of daily occupational habits and balance, having resulted in compromised physical and mental health. During this physical distancing period, occupational therapists in Yunnan Province of China delivered a health promotion programme using WeChat, an online platform. The main purpose of the programme was to support the redesigning of a person's lifestyle in the face of the pandemic, as well as to enable participation in occupations that foster their self-efficacy and mental wellbeing. During the self-quarantine period, the programme was accessed frequently, with viewers spanning from practicing therapists to the general public. Findings from WeChat analytics and follow up interviews with programme viewers suggested that internet-based health promotion programme can be effective in places where internet is commonly used by the general public.

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Introduction: To explore the pathogenesis of gestational diabetic nephropathy (GDM) and its possible biological function by using large data bioinformatics mining algorithm. Materials and methods: The Gene Expression Omnibus (GEO) was retrieved and the data of GDM differential expression chip were screened and downloaded. The differentially expressed genes were screened by using R software Lima package (Log2FC > 1; P < 0.05). Functional enrichment of differentially expressed genes was performed. Protein–protein interaction network of GDM pathogenesis was constructed by the database (STRING) to analyze the interaction between differentially expressed gene-coding proteins. Using Cytohubb software to further screen the key genes (hub genes) in the signaling pathway. In next step, 35 case of GDM and 39 normal pregnant women were selected as subjects. The expression levels of key gene coding proteins in venous blood and placenta tissues of GDM and normal pregnant women detected by immunohistochemical and qRT-PCR. And using cell experiment to analysis the key gene’s effects in GDM. Results: By Bioinformatics Analysis, CDK1 was significantly depressed in GDM (P <0.001), In clinical data, CDK1 protein and mRNA expressions were also significantly down-regulation in GDM compared with NC (P <0.001). In vitro study, with high glucose treatment, the cell were hyperproliferation with CDK1 depressing and AKT overexpression (P <0.001). However, with CDK1 supplement, the cell returned to normal with CDK1 overexpression and AKT depressing (P <0.001). Conclusion: CDK1 is differentially expressed in patients with GDM and play a key part in occurrence and development of GDM. CDK1 may be a key target for treatment and prevention of GDM.

IntroductionDue to the difficulty of early diagnosis, nearly 70% of ovarian cancer patients are first diagnosed at an advanced stage. Thus, improving current treatment strategies is of great significance for ovarian cancer patients. Fast-developing poly (ADP-ribose) polymerases inhibitors (PARPis) have been beneficial in the treatment of ovarian cancer at different stages of the disease, but PARPis have serious side effects and can result in drug resistance. Using PARPis in combination with other drug therapies could improve the efficacy of PRAPis.In this study, we identified Disulfiram as a potential therapeutic candidate through drug screening and tested its use in combination with PARPis.MethodsCytotoxicity tests and colony formation experiments showed that the combination of Disulfiram and PARPis decreased the viability of ovarian cancer cellsResultsThe combination of PARPis with Disulfiram also significantly increased the expression of DNA damage index gH2AX and induced more PARP cleavage. In addition, Disulfiram inhibited the expression of genes associated with the DNA damage repair pathway, indicating that Disulfiram functions through the DNA repair pathway.DiscussionBased on these findings, we propose that Disulfiram reinforces PARPis activity in ovarian cancer cells by improving drug sensitivity. The combined use of Disulfiram and PARPis provides a novel treatment strategy for patients with ovarian cancer.