Conectar
by Qian Liu, Yuanhao Peng, Wenbin Liu, Xiangjian Luo
Cervical cancer remains the second leading cause of female cancer mortality worldwide, with metastasis representing a critical therapeutic challenge. This study systematically reveals the key role of SERPINH1 (Serpin Family H Member 1) as a hub regulator of malignant progression in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). Through analysis of TCGA-CESC datasets, we identified that high SERPINH1 expression is significantly correlated with poor prognosis and contributes to tumor progression by promoting cell proliferation, invasion, and metastatic phenotypes. In vitro experiments validated these findings, demonstrating that SERPINH1 overexpression markedly enhanced the proliferation, invasion, and metastasis of cervical cancer cells, whereas its knockdown substantially inhibited these processes. Furthermore, based on the SERPINH1-related differentially expressed genes, a prognostic risk model was constructed, successfully identifying PLOD1, ITGA5, and ESM1 as core collaborative genes affecting patient prognosis. Overall, our findings underscore the multiple functions of SERPINH1 as a hub for cervical cancer metastasis regulation, suggesting its potential as a promising biomarker for tailoring strategies in metastasis patients of CESC.
To determine the effectiveness of brief reminiscence-based psychosocial interventions in alleviating psychological distress in cancer patients.
Cancer patients suffer tremendous psycho-spiritual pain, which affects their quality of life. Brief reminiscence-based psychosocial interventions have demonstrated positive effects on the mental health of cancer patients; however, the efficacy of these interventions has been inconsistent.
A systematic review and meta-analysis.
This review was conducted and reported in accordance with the PRISMA 2020 checklist provided by the EQUATOR network. The Cochrane Library, Web of Science, PsycINFO, PubMed, Embase, CINAHL and Scopus databases were systematically searched from inception to 27 November 2022 to identify randomised controlled trials (RCTs) published in English.
Twenty studies involving 1744 cancer participants were included. The meta-analysis showed statistically significant effects of brief reminiscence-based psychosocial interventions on hope, anxiety and depression at post-intervention. A separate analysis revealed that brief reminiscence-based psychosocial interventions had a sustainable effect on hope, spiritual well-being, anxiety and depression at 1 month after the intervention. However, no statistically significant effect on quality of life was found in our study either immediately after the intervention or at 1 month.
Brief reminiscence-based psychosocial interventions can significantly reduce anxiety and depressive symptoms and improve hope and spiritual well-being in cancer patients.
This study further supports that brief reminiscence-based psychosocial interventions should be incorporated into the routine care of cancer patients to address their psychosocial distress.
All authors of this article contributed to the study conception and design. All authors of the included studies provided original data for this paper.
This study focused on unravelling the role of PCAT-1 in wound-healing process, particularly its impact on regenerative and osteogenic abilities of mesenchymal stem cells (MSCs). We delved into how PCAT-1 regulates mitochondrial oxidative phosphorylation (OXPHOS) and interacts with pivotal molecular pathways, especially β-catenin and PKM2, using human bone marrow-derived MSCs. MSCs were cultured under specific conditions and PCAT-1 expression was modified through transfection. We thoroughly assessed several critical parameters: MSC proliferation, mitochondrial functionality, ATP production and expression of wound healing and osteogenic differentiation markers. Further, we evaluated alkaline phosphatase (ALP) activity and mineral deposition, essential for bone healing. Our findings revealed that overexpressing PCAT-1 significantly reduced MSC proliferation, hampered mitochondrial performance and lowered ATP levels, suggesting the clear inhibitory effect of PCAT-1 on these vital wound-healing processes. Additionally, PCAT-1 overexpression notably decreased ALP activity and calcium accumulation in MSCs, crucial for effective bone regeneration. This overexpression also led to the reduction in osteogenic marker expression, indicating suppression of osteogenic differentiation, essential in wound-healing scenarios. Moreover, our study uncovered a direct interaction between PCAT-1 and the PKM2/β-catenin pathway, where PCAT-1 overexpression intensified PKM2 activity while inhibiting β-catenin, thereby adversely affecting osteogenesis. This research thus highlights PCAT-1's significant role in impairing wound healing, offering insights into the molecular mechanisms that may guide future therapeutic strategies for enhancing wound repair and bone regeneration.
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