Profilin 2 (PFN2) functions as an actin cytoskeleton regulator and serves an important role in cell motility. However, a role for PFN2 in the progression of colorectal cancer (CRC), particularly in metastasis, has yet to be clarified. The aim of the present study was to investigate whether PFN2 served specific roles in the progression of human CRC. The results demonstrated that PFN2 was differentially expressed in CRC tissues and cell lines by reverse transcription-quantitative polymerase chain reaction and western blotting. PFN2 expression was also negatively associated with the degree of tumor metastasis. Low PFN2 expression in CRC cells was related with enhanced epithelial-mesenchymal transition (EMT) and, in turn, may increase migratory capabilities. Overexpression of PFN2 in CRC cell lines with a low level of endogenous PFN2 inhibited the EMT process, as well as the associated migration; in addition, myosin light chain (MLC) phosphorylation was upregulated. Inhibition of MLC phosphorylation attenuated the inhibition of EMT and cell migratory abilities induced by PFN2 overexpression in CRC cell lines, the results suggested that PFN2 may suppress cancer EMT and the subsequent metastasis by regulating cytoskeletal reorganization. These results demonstrated that PFN2 may serve a suppressive role in the metastasis of CRC and therefore may provide a new potential target for cancer therapeutics.
Nursing is a vital health profession. In almost all clinical and hospital settings, nurses offer primary palliative care. Nurses are recognized for their strong philosophy of care for a wide spectrum of disorders. No matter the sickness, condition, or clinical situation, palliative care is considered essential in nursing practice. Palliative care nursing is the provision of palliative care services to cancer patients and their families, regardless of whether cancer can be cured or not. A large body of evidence shows that early palliative care nursing integration improves the quality of life and survival of cancer patients. Due to the intricacy of cancer, the landscape of cancer care is shifting. Cancer is a life-threatening disease with a high mortality rate. Oncology nurses’ skills and experience are vital in providing specialized patient care and fulfilling the needs of patients and their families. The current study examines the shifting environment of palliative care nursing in oncology. However, new palliative care nursing approaches are required to adapt to the evolving cancer scenario.
ObjectiveThe observational studies indicate an association between obesity and epilepsy, but it is unclear whether such an association responds to causality. The objective of this study was to determine the causal relationship between obesity and fat distribution and epilepsy subtypes based on waist circumference, hip circumference (HP), waist-hip ratio (WHR), and body mass index (BMI).MethodsA two-sample Mendelian randomization study was conducted separately for the four indicators of obesity and epilepsy and its seven subtypes, with reverse Mendelian randomization and multivariate Mendelian randomization for significant outcomes.ResultsA two-sample Mendelian randomized analysis informed us that waist circumference was a risk factor for juvenile myoclonic epilepsy (beta = 0.0299, P = 4.60 × 10−3). The increase in hip circumference increased the risk of juvenile myoclonic epilepsy and epilepsy, with effect values of 0.0283 (P = 2.01 × 10−3) and 0.0928 (P = 1.40 × 10−2), respectively. Furthermore, children with a higher BMI exhibit a higher risk of epilepsy (beta = 0.0148 P = 1.05 × 10−3). The reverse Mendelian randomization study revealed that childhood absence epilepsy increased its BMI (beta = 0.8980, P = 7.52 × 10−7), and juvenile myoclonic epilepsy increased its waist circumference (beta = 0.7322, P = 3.26 × 10−2). Multivariate Mendelian randomization revealed that an increase in hip circumference and waist-hip ratio increased the risk of juvenile myoclonic epilepsy, with an effect value of 0.1051 (P = 9.75 × 10−4) and 0.1430 (P = 3.99 × 10−3), respectively, while an increase in BMI and waist circumference instead decreased their risk, with effect values of −0.0951 (P = 3.14 × 10−2) and−0.0541 (P = 1.71 × 10−2). In contrast, multivariate Mendelian randomization for childhood absence epilepsy and epilepsy did not identify any independent risk factors.SignificanceOur findings provide novel evidence in favor of obesity as a risk factor for epilepsy and waist circumference as a risk factor for juvenile myoclonic epilepsy. Increased hip circumference confers an elevated risk of juvenile myoclonic epilepsy and epilepsy (all documented cases), and a high BMI increases the risk of childhood absence epilepsy. With this, new insights are provided into the energy metabolism of epilepsy, which supports further nutritional interventions and the search for new therapeutic targets.
Diabetes has been linked to an increased risk of epilepsy in observational studies. The antiglycemic drugs have been shown in animal studies to improve seizures. However, whether the associations between antiglycemic drugs and epilepsy in human is not known. In this study, we conducted a Mendelian randomization investigation to assess the potential causal role of antiglycemic drug targets in epilepsy.We used the International League Against Epilepsy Data as the discovery set and FinnGen Data as the replication set .Three antidiabetic drug target genes, including ETFDH, CYP21A2, and CYP2D6 were discovered to be involved in epilepsy. ETFDH predicted as a target gene in the discovery set (IVW, OR = 1.018, 95% CI, 1.004–1.033, p = 0.009), replication set (IVW, OR = 1.074, 95% CI, 1.034–1.114, p = 0.00016) and CYP21A2 gene in the discovery set (IVW, OR = 1.029, 95% CI, 1.005– 1.053, p = 0.016) and replication set (IVW, OR = 1.057, 95% CI, 1.001–1.116, p = 0.045) showed a causal association with an increased risk of epilepsy. In contrast, the CYP2D6 gene was found to be a protective factor for epilepsy in both the discovery set (IVW, OR = 0.0984, 95% CI, 0.969–0.998, p = 0.025) and the replication set (IVW, OR = 0.977, 95% CI, 0.955–1.000, p = 0.046). By searching the pharmacological effects of anti-glucose drug target gene related drugs and binding drugs in DrguBank, Metformin was found to be ETFDH gene inhibitor, showing a potential therapeutic effect on epilepsy.
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