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Purpose: Combinatorial therapies are essential for treating advanced non-small cell lung cancer (NSCLC), particularly overcoming resistance to third-generation epidermal growth factor receptor (EGFR) like osimertinib (OSI). The Hippo signaling pathway, a critical regulator of cell proliferation, apoptosis, and tumor progression, is often dysregulated in NSCLC and contributes to chemo-resistance. This study investigated the potential of epigallocatechin-3-gallate (EGCG), a green tea polyphenol, to overcome OSI resistance by modulating the Hippo signaling pathway, specifically through inhibition of the YAP-1 (Yes-associated protein)-TEAD (TEA domain transcription factor)-CTGF (connective tissue growth factor) axis.

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Despite significant advancements in the treatment of non-small cell lung cancer (NSCLC) using conventional therapeutic methods, drug resistance remains a major factor contributing to disease recurrence. In this study, we aimed to explore the potential benefits of combining PI3K inhibition with Cisplatin in the context of NSCLC-derived A549 cells. Human non-small cell lung cancer A549 cells were cultured and treated with BKM120, cisplatin, or their combination.

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Background: This study seeks to provide preclinical evidence demonstrating the potential of Antrocinol, a derivative of antrocin derived from the active compound of Antrodia cinnamomea, as a promising small-molecule drug candidate for overcoming drug-resistant hepatocellular carcinoma (HCC).

Methods: We developed Lenvatinib-resistant Huh-7 and HepG cell lines (Huh-7/LR, HepG2/LR) to evaluate their viability and apoptotic response to Antrocinol. Autophagy-dependent cell death was assessed in Huh-7/LR cells using Z-VAD-FMK and shATG5 transfection.

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Caulerpin, a bisindole alkaloid derived from green algae of the genus Caulerpa, has exhibited a promising anti-proliferative effect on various tumor cells in vitro. However, its pharmacological potential has not been intensively explored in cervical cancer. In this study, the antitumor property of caulerpin was assessed in cervical cancer cells (HeLa and SiHa cells) and xenograft mouse models.

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2-Deoxy-D-Glucose and ES-936 sensitize cancer- but not normal cells to both low- and high LET irradiation.

Front Oncol

August 2025

Department of Biophysics, GSI Helmholtzzentrum für Schwerionenforschung, Darmstadt, Germany.

Introduction: Metabolic differences of normal- and cancer cells represent an important target for the development of novel cancer treatment strategies. Given that radiotherapy constitutes one of the primary treatment modalities for solid cancers, the targeting of cancer cell metabolism to enhance their sensitivity to irradiation emerges as a promising approach. The utilization of glycolysis even under aerobic conditions in cancer cells presents a unique target to deprive cancer cells of energy and metabolites required not only for their rapid cell growth but also for the repair of irradiation induced DNA damage.

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