Previous observational studies have inconsistently suggested that poor sleep is a novel risk factor for breast cancer (BC). However, these studies mainly focused on sleep duration; other sleep domains were rarely reported. The aim of this study was to evaluate the association of a broad range of sleep domains with the risk of BC incidence. We used a community-based 1 : 1 individual matched case-control design that included 401 female patients with incident BC and 401 age-matched and area-matched female controls in Jiujiang, China. Long-term sleep habits were assessed comprehensively using a validated 17-item Sleep Factors Questionnaire. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression. Light exposure at night (highest vs. lowest level, aOR=1.19, 95% CI: 1.06-2.68), habitual timing of sleep (after 12 a.m. midnight vs. before 22 p.m., aOR=1.12, 95% CI: 1.03-2.62), night/shift work (yes vs. no, aOR=1.38, 95% CI: 1.04-2.71), and frequency of night-time wakings (>2 per night vs. never, aOR=1.21, 95% CI: 1.10-2.96) were associated with an increased risk of BC after mutually adjusting for other sleep parameters. These positive associations remained irrespective of menopausal status and tumor estrogen receptor status. There was no association between sleep duration, sleep quality, sleep medication use, insomnia frequency, daytime nap, and the risk of BC. Our results indicate that sleep problems including light exposure at night, night/shift work, late sleeping, and frequent night waking could increase the risk of BC development, independent of other sleep factors.
Background: Histone deacetylase (HDAC) is closely related to the occurrence and development of breast cancer (BC). Its inhibitor (HDACi) has been used to treat BC, while the e cacy of clinical trials was not reached expectations. HDACi combined with other drugs may be an effective strategy. This study explored the effect of HDACitucidinostat combined with selinexor, anexportin 1 (XPO1) inhibitor, on BC cellsin vitro.Methods: BC cell lines of MCF-7 (wt-TP53), MDA-MB-175 (wt-TP53), MDA-MB-134 (mut-TP53), T47D (mut-TP53) were cultured. The IC 50 values of tucidinostat and selinexor on BC cells were calculated. The effects of tucidinostat and selinexor on proliferation, invasion and apoptosis of BC cells were observed accordingly. Western blotting was used to detect the protein expressions of p53, p21, Cyclin D1, Bcl-2 and Bax.Results:Compared with mut-TP53 BC, both tucidinostat and selinexor showed better inhibitory activitiesonwt-TP53 BC including MCF-7 and MDA-MB-175. Tucidinostat combined with selinexor signi cantly improved the effects of tucidinostat alone on the proliferation and invasion inhibitions and apoptosis promotionsof MCF-7 and MDA-MB-175 cells in vitro. It also signi cantly enhanced the effects of tucidinostat on up-regulating the expression levels of acetyl-p53, nuclear p53, total p53, p21 and Bax, and down-regulating the expression levels of Cyclin D1 and Bcl-2 in MCF-7 or MDA-MB-175 cells.Conclusion: Taken together, we believe that tucidinostat and selinexor are potentially effective drug combinations for the treatment of wt-TP53 BC, and the molecular mechanism may be throughenhancing the activity of p53 in the nucleus of BC cells to suppress proliferation and invasion and promote apoptosis of BC cells.
Environmental issues have received worldwide attention in recent years, and a large body of literature has focused on environmental regulations and business innovation. However, very few studies examine the effects of market-incentive-based environmental regulation policies on the quality of corporate innovation. Thus, this paper uses China’s A-share listed enterprises in 2010–2020 and China’s carbon trading policy (CCTP) to conduct a quasi-natural experiment. The results show that the CCTP significantly increases the quality of innovation but does not affect the quantity of firm innovation. Furthermore, according to the result of heterogeneity analysis, the effect of CCTP on high-quality innovation occurs mainly in low-financialization and non-state enterprises.
Background: Histone deacetylase (HDAC) is closely related to the occurrence and development of breast cancer (BC). Its inhibitor (HDACi) has been used to treat BC, while the efficacy of clinical trials was not reached expectations. HDACi combined with other drugs may be an effective strategy. This study explored the effect of HDACitucidinostat combined with selinexor, anexportin 1 (XPO1) inhibitor, on BC cellsin vitro. Methods: BC cell lines of MCF-7 (wt-TP53), MDA-MB-175 (wt-TP53), MDA-MB-134 (mut-TP53), T47D (mut-TP53) were cultured. The IC50 values of tucidinostat and selinexor on BC cells were calculated. The effects of tucidinostat and selinexor on proliferation, invasion and apoptosis of BC cells were observed accordingly. Western blotting was used to detect the protein expressions of p53, p21, Cyclin D1, Bcl-2 and Bax.Results:Compared with mut-TP53 BC, both tucidinostat and selinexor showed better inhibitory activitiesonwt-TP53 BC including MCF-7 and MDA-MB-175. Tucidinostat combined with selinexor significantly improved the effects of tucidinostat alone on the proliferation and invasion inhibitions and apoptosis promotionsof MCF-7 and MDA-MB-175 cells in vitro. It also significantly enhanced the effects of tucidinostat on up-regulating the expression levels of acetyl-p53, nuclear p53, total p53, p21 and Bax, and down-regulating the expression levels of Cyclin D1 and Bcl-2 in MCF-7 or MDA-MB-175 cells. Conclusion: Taken together, we believe that tucidinostat and selinexor are potentially effective drug combinations for the treatment of wt-TP53 BC, and the molecular mechanism may be throughenhancing the activity of p53 in the nucleus of BC cells to suppress proliferation and invasion and promote apoptosis of BC cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.