RESUMO
Aims: Prostate cancer patients face impaired body image and psychological distress during the diagnosis and treatment of the disease, which leads to changes in mood, cognition and behavior. Psychological resilience has been shown to buffer shocks and stresses from the disease. Therefore, this study investigates the relationship between family functioning and psychological resilience in prostate cancer patients and the mediating role of self-efficacy between family functioning and psychological resilience to provide a relevant theoretical basis for improving patients' psychological status by providing relevant theoretical basis. Method: Using a cross-sectional design, participants were 215 patients with prostate cancer admitted to and treated in a tertiary hospital in Jiangsu province, China. Questionnaires were administered using the general information questionnaire, the Connor-Davidson Resilience Scale (CD-RISC), the Family Adaptation, Partnership, Growth, Affection, and Resolution Index (APGAR), and the General Self-efficacy Scale (GSES). Data were analyzed using descriptive and correlational analyses and the bootstrap mediation test was used to test the effect relationship between the variables. Results: Family functioning, self-efficacy and psychological resilience were significantly and positively correlated (r = 0.526, P < 0.01; r = 0.378, P < 0.01; r = 0.358, P < 0.01). The mediating effect of psychological resilience between family functioning and psychological resilience was significant, accounting for 42.56%. Conclusion: Family function and self-efficacy have been shown to increase the level of psychological resilience in prostate cancer patients. Attention should be paid to the mental health problems of prostate cancer patients, early screening and intervention, and the use of patients' family resources to improve their confidence in recovering from the disease, thus increasing their psychological resilience and improving their mental health.
RESUMO
Decreased expression of epithelial cadherin (E-cadherin) has been noted to associate with aggressiveness and metastasis of breast cancer. The aim of this study was to examine the effect of C-Terminal EH domain-containing protein 2 (EHD2) expression on E-cadherin and related mechanism in the metastasis of breast cancer. Immunohistochemical analysis was performed in 96 human breast carcinoma samples and the data were correlated with clinicopathologic characteristics. Furthermore, Western blot analysis was performed for EHD2 and E-cadherin in breast carcinoma samples and cell lines to evaluate their protein levels and molecular interaction. We found that the expression of EHD2 was positively related with E-cadherin expression (P < 0.01), moreover, EHD2 expression was significantly correlated with histologic grade (P < 0.01). Meanwhile, E-cadherin expression obtained similar results. Kaplan-Meier survival analysis showed that decreased expression of EHD2 and E-cadherin exhibited a significant correlation with poor prognosis in human breast cancer (P < 0.01). While in vitro, we employed siRNA technique to knock down EHD2 expressions and observed their effects on breast cancer cells growth. EHD2 depletion by siRNA promoted PCNA expression, and it was concurrent with the decreased expression of epithelial marker E-cadherin and the increased expression of N-cadherin by Western blot analysis. Consistent with these observations, the suppression of EHD2 in breast cancer cells remarkably promoted cellular proliferation and migration. On the basis of these results, we suggested that EHD2 can inhibit the metastasis of human breast cancer by regulating the EMT key markers E-cadherin and N-cadherin.