FZKA reverses gefitinib resistance by regulating EZH2/Snail/EGFR signaling pathway in lung adenocarcinoma

Tang, Qing; Xu, Mengfei; Long, Shunqin; Yu, Yaya; Ma, Changju; Wang, Rui; Li, Jing; Wang, Xi; Fang, Fang; Han, Ling; Wu, Wanyin; Wang, Sumei

doi:10.1016/j.jep.2023.116646

Cited by 3 publications

(2 citation statements)

References 41 publications

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“…In addition, in vivo nude mouse tumor transplantation experiments also showed that the combination of QJYFMF and GE can effectively reduce the tumor growth rate. This is similar to the previously reported results of FZKA inhibiting lung adenocarcinoma cell growth, proliferation, and invasion and reversing GEtreatment resistance of lung adenocarcinoma [21]. These results suggested that combining with QJYFMF may have a signi cant synergistic effect on GE treatment of NSCLC.…”

Section: Discussionsupporting

confidence: 91%

Investigating the Mechanism of Qingjie Yifei Miao Fang in Synergistic Treatment of Non-Small Cell Lung Cancer with Gefitinib Based on the PTEN/PI3K/AKT Signaling Pathway

Tang,

Pan,

Xiao

et al. 2024

Preprint

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Background: To investigate the mechanism of Qingjieyifei Miao Fang (QJYFMF) combined with gefitinib (GE) against non-small cell lung cancer (NSCLC). Methods: Network pharmacology was applied to obtain the key targets and signaling pathways of QJYFMF in NSCLC treatment. An A549 cell culture model of QJYFMF and a mouse model of lung cancer surface transplantation were established in vivo and in vitro, respectively. The therapeutic effect of QJYFMF on NSCLC was investigated by CCK-8, flow cytometry, wound healing, and transwell assay. The expression of key proteins in the PTEN/PI3K/AKT signaling pathway was verified by western blot and qRT-PCR assay. Results: A total of 98 active components and 901 targets of QJYFMF were obtained, which were mainly concentrated in the PI3K-AKT, MARK, and apoptosis signaling pathways. Compared with the control group, QJYFMF significantly inhibited the A549 cell proliferation rate, promoted cell apoptosis, and reduced the A594 cell migration and invasion abilities. Furthermore, the transplanted tumor volume and weight were decreased, the PTEN, caspase-9, and BAD protein expression levels were increased, the PI3K/p-PI3K, AKT/p-AKT, p-caspase-9 and p-BAD expression levels were decreased, and the BAD and caspase-9 mRNA expression levels were increased. The combined use of GE+QJYFMF displayed greater efficacy. Conclusion: QJYFMF significantly inhibited NSCLC proliferation, migration, and invasion and promoted cell apoptosis. The combination of GE+QJYFMF can increase the efficacy of GE, and the mechanism may be through the PTEN/PI3K/AKT signaling pathway.

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Section: Discussionsupporting

confidence: 91%

Investigating the Mechanism of Qingjie Yifei Miao Fang in Synergistic Treatment of Non-Small Cell Lung Cancer with Gefitinib Based on the PTEN/PI3K/AKT Signaling Pathway

Tang,

Pan,

Xiao

et al. 2024

Preprint

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“…EZH2 is a commonly overexpressed gene in various cancers , and its high expression levels are frequently associated with adverse prognosis [35][36][37][38]. In addition to its role in regulating H3K27 trimethylation [39], EZH2 is also capable of regulating its downstream targets in a PRC2-and methylation-independent manner.…”

Section: The Relationship Between Ezh 2 Expression Levels In Glioma T...mentioning

confidence: 99%

Overexpression of EZH2 is associated with clinicopathological parameters and poor prognosis in gliomas

Peng,

Chen,

Yang

et al. 2024

Preprint

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Histone methyltransferase EZH2, primarily localized in the nucleus, mediates constitutive Polycomb repressive complex activity by trimethylating lysine 27 of histone H3 (H3K27me3), leading to gene silencing through canonical and noncanonical mechanisms, resulting in transcriptional repression or activation. Its involvement is crucial in cell growth, proliferation, differentiation, and apoptosis, with its effects linked to the regulation of various targets and signaling pathways. Overexpression of EZH2 alters gene expression and function, thereby facilitating cancer progression. Recent research has identified the potential prognostic role of EZH2 expression in glioma patients. This study assesses the clinicopathological significance and prognostic value of EZH2 expression in gliomas using available data. The mRNA levels of EZH2 in tumor tissues and normal tissues were assessed using timer2.0 and data from CGCA and TGCA. The prognostic significance of EZH2 mRNA expression was determined using Kaplan-Meier plotter. A total of 147 clinical samples from glioma patients underwent immunohistochemistry analysis to evaluate EZH2 protein expression. Cox proportional hazards regression model and Kaplan-Meier survival curves were employed to assess the relationship between EZH2 expression, clinicopathological parameters, and overall survival (OS). Across multiple tumor cohorts, EZH2 was found to be upregulated and amplified in tumor tissues. In high-grade glioma patients, EZH2 expression was significantly increased, and higher EZH2 expression correlated with poorer OS, disease-specific survival (DSS), and progression-free interval (PFI). Therefore, the level of EZH2 may serve as a prognostic biomarker for glioma patients.

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Strategies for enhancing non-small cell lung cancer treatment: Integrating Chinese herbal medicines with epidermal growth factor receptor-tyrosine kinase inhibitors therapy

Chen,

et al. 2024

European Journal of Pharmacology

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FZKA reverses gefitinib resistance by regulating EZH2/Snail/EGFR signaling pathway in lung adenocarcinoma

Cited by 3 publications

References 41 publications

Investigating the Mechanism of Qingjie Yifei Miao Fang in Synergistic Treatment of Non-Small Cell Lung Cancer with Gefitinib Based on the PTEN/PI3K/AKT Signaling Pathway

Investigating the Mechanism of Qingjie Yifei Miao Fang in Synergistic Treatment of Non-Small Cell Lung Cancer with Gefitinib Based on the PTEN/PI3K/AKT Signaling Pathway

Overexpression of EZH2 is associated with clinicopathological parameters and poor prognosis in gliomas

Strategies for enhancing non-small cell lung cancer treatment: Integrating Chinese herbal medicines with epidermal growth factor receptor-tyrosine kinase inhibitors therapy

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