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Objective To explore the exposure of decarbromo diphenyl ether (BDE-209), a new persistent organic pollutant (POP) with the highest level in human body, on the migration of triple-negative breast cancer (TNBC) cell line MDE-MB-231, and explore the effects of its exposure on the development of TNBC and underlying mechanism in the process. Methods MDA-MB-231 cells were divided into blank control group (high glucose DMEM), solvent control group (2% DMSO in high glucose DMEM) and BDE-209 exposure groups (0.02, 0.2, 2, 20, 200 and 2 000 ng/mL BDE-209 in high glucose DMEM).In 24 h after culture, CCK-8 assay was used to determine the IC50 value of BDE-209.Scratch wound assay and Transwell assay were employed to determine the effect of BDE-209 exposure on migration ability of MDA-MB-231 cells.The protein levels of signal transducers and activators of transcription 3(STAT3) and its phosphorylation level (p-STAT3) were detected with Western blotting and immunocytochemical assay.The effect of BDE-209 exposure on the expression and activation of STAT3 in tumor-bearing mice with transplantation of 4T1 cells. Results BDE-209 exposure significantly promoted the migration of MDA-MB-231 cells, in a dose-dependent manner, when compared with blank control cells (P < 0.01).Western blotting and immunocytochemical assay showed that BDE-209 exposure enhanced the expression of STAT3 and p-STAT3 in MDA-MB-231 cells (P < 0.05).In tumor-bearing mice, the expression levels of STAT3 and p-STAT3 were obviously enhanced in the TNBC tissues after exposure to 200 ng/mL BDE-209.While, treatment of STAT3 inhibitor STAT3-IN-1 could notably suppress the migration of MDA-MB-231 cells induced by BDE-209 exposure (P < 0.001). Conclusion BDE-209 exposure promotes the migration ability of TNBC cells via up-regulation and activation of STAT3, and thus improve the metastasis.

Objectives: This study aimed to investigate the factors that impact the readiness and success of kidney cancer survivors returning to work, providing insights for healthcare professionals, employers, and policymakers., Methods: A prospective longitudinal study was conducted at Sun Yat-sen University Cancer Center from April 2022 to June 2023. The study enrolled 282 kidney cancer survivors aged 18 to 60 who completed three surveys at 1, 3, and 6 months postsurgery. Data collection involved telephone interviews and self-administered questionnaires, capturing sociodemographic information, medical history, and employment status, while follow-up assessments tracked return-to-work readiness. The scales used for analysis included the Generalized Anxiety Disorder Scale, the Patient Health Questionnaire, the Return-to-Work Self-Efficacy Questionnaire, the Perceived Social Support Scale, and the Brief Fatigue Inventory. Generalized Estimation Equations were applied to identify significant factors, with both single-factor and multivariate analyses performed to pinpoint the most critical variables., Results: Return-to-work rates at 1, 3, and 6 months postsurgery were 26.9%, 59.9%, and 76.2%, respectively. Higher levels of anxiety, lower self-efficacy, older age, and greater fatigue were associated with reduced return-to-work rates. Physically demanding jobs posed more barriers compared to nonmanual roles. Significant factors identified in multivariate analysis included anxiety, self-efficacy, fatigue, and the nature of the patient's work., Conclusion: Psychological, physical, and job-related factors play a crucial role in determining whether kidney cancer survivors can successfully return to work. Tailored support and flexible work arrangements could help kidney cancer survivors reintegrate into the workforce, leading to better long-term outcomes., Implication for Nursing Practice: Nursing professionals can play a vital role in assessing and supporting kidney cancer survivors during their recovery process by addressing both psychological and physical factors. Incorporating return-to-work readiness into postoperative care plans, offering mental health support, and liaising with employers to create flexible working conditions could enhance the reintegration of survivors into the workforce., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Objectives: To investigate the effect of decarbromodiphenyl ether (BDE-209) exposure on the migration ability of triple-negative breast cancer (TNBC) cells and to explore the underlying mechanism., Methods: Human TNBC MDA-MB-231 cells were divided into blank control group and BDE-209 exposure groups (treated with 0.02, 0.20, 2.00, 20.00 and 200.00 ng/mL BDE-209 in high glucose DMEM). Extracellular vehicles (EVs) secreted by MDA-MB-231 cells were isolated by differential ultracentrifugation. Transmission electron microscopy (SEM), nanoparticle tracking analysis (NTA) and Western blotting were performed to characterize the EVs. The effect of the EVs induced by BDE-209 exposure (EVs-BDE-209) on the migration and invasion of MDA-MB-231 cells was detected by wound-healing assay and Transwell test. qRT-PCR was used to measure the miR-221 level in EVs-BDE-209. The expression of MMP9 in MDA-MB-231 cells was determined by Western blotting., Results: Compared with the blank control, BDE-209 exposure increased the tumor cell-derived EVs in dose-dependent manner. The MDA-MB-231 cells co-cultured with EVs released by 200.00 ng/mL BDE-209 exposure showed an 86% increase in cell migration rate, a 1.32-fold higher number of membrane-penetrating cells, a 2.71-fold higher expression level of miR-221, and a 1.62-fold higher expression level of MMP9 compared with the blank control group (all P <0.05). While transfection with anti-miR-221 antibody to decrease miR-221 level in EVs significantly reversed the increased invasion ability of the MDA-MB-231 cells treated with EVs-BDE-209., Conclusions: BDE-209 exposure may promote metastasis potential of MDA-MB-231 cells via EVs-BDE-209 transmitted miR-221.