Translational cancer research · 2026
Si Ni Powder enhances chemotherapy efficacy in sleep-deprived breast cancer via modulation of the tumor microenvironment.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Jia Heyuan, Chen Ying, Cheng Hao, Yao Surui, Wang Qingwen, Qian Mengyuan, Ge Cun, Huang Zhaohui, Chen Yanyan
Аннотация
BACKGROUND: Sleep disturbance, affecting up to 62% of breast cancer patients undergoing chemotherapy (CT), contributes to chemoresistance and tumor progression. However, the underlying mechanisms and potential interventions remain poorly defined. While Si Ni Powder (SNP) is known for its sleep-improving properties, its ability to mitigate CT resistance induced by sleep deprivation (SD) is unexplored. In this study, we aimed to investigate whether SNP could improve sleep, enhance the efficacy of doxorubicin (Dox) under SD conditions, and modulate tumor microenvironment (TME) remodeling.
METHODS: An orthotopic 4T1 breast cancer mouse model was used to evaluate the impact of SD on the efficacy of Dox and to assess the therapeutic potential of SNP. Tumor growth, serum melatonin (MT), and cortisol (Cor) levels were monitored. Ultra-high performance liquid chromatography-quadrupole-orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS) was employed to characterize the chemical constituents of SNP and to identify the compounds absorbed into tumor tissues. Transcriptomics, network pharmacology, and molecular docking were integrated to elucidate the underlying mechanisms.
RESULTS: SD weakened the antitumor effect of Dox, which was effectively rescued by SNP. SD activated inflammatory signaling, extracellular matrix (ECM) remodeling, and lipid metabolic pathways, all of which were counteracted by SNP. A total of 168 chemical components were identified in SNP and 20 SNP-derived components were detected in tumor tissues. Integrated analyses revealed a multi-target regulatory network involving six key targets, including Stat3, Stat6, Ppara, Rxra, Ar, and Hes1. Molecular docking suggested strong interactions between these targets and five potential active compounds, namely neoeriocitrin, genistein, hesperetin, formononetin, and tetrahydroxyflavanone.
CONCLUSIONS: SNP counteracts SD-induced chemoresistance via multi-faceted modulation of the TME, encompassing inflammatory suppression, normalization of the ECM, and reprogramming lipid metabolism.
METHODS: An orthotopic 4T1 breast cancer mouse model was used to evaluate the impact of SD on the efficacy of Dox and to assess the therapeutic potential of SNP. Tumor growth, serum melatonin (MT), and cortisol (Cor) levels were monitored. Ultra-high performance liquid chromatography-quadrupole-orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS) was employed to characterize the chemical constituents of SNP and to identify the compounds absorbed into tumor tissues. Transcriptomics, network pharmacology, and molecular docking were integrated to elucidate the underlying mechanisms.
RESULTS: SD weakened the antitumor effect of Dox, which was effectively rescued by SNP. SD activated inflammatory signaling, extracellular matrix (ECM) remodeling, and lipid metabolic pathways, all of which were counteracted by SNP. A total of 168 chemical components were identified in SNP and 20 SNP-derived components were detected in tumor tissues. Integrated analyses revealed a multi-target regulatory network involving six key targets, including Stat3, Stat6, Ppara, Rxra, Ar, and Hes1. Molecular docking suggested strong interactions between these targets and five potential active compounds, namely neoeriocitrin, genistein, hesperetin, formononetin, and tetrahydroxyflavanone.
CONCLUSIONS: SNP counteracts SD-induced chemoresistance via multi-faceted modulation of the TME, encompassing inflammatory suppression, normalization of the ECM, and reprogramming lipid metabolism.