Ovarian cancer is a prevalent malignancy in the female reproductive system, representing a significantly fatal and incurable tumor. Chelerythrine (CHE), a natural benzopyridine alkaloid, has demonstrated a broad spectrum of anticancer activities. Nevertheless, the ovarian cancer inhibitory impact of CHE remains unclear. In this study, we investigated the cytotoxic mechanism and potential targets of CHE on in vitro cultures of A2780 and SKOV3 cells derived from ovarian cancer. Additionally, in vivo experiments were conducted to confirm the suppressive impact of CHE on tumor growth in nude mice. The findings revealed that CHE impeded the growth of A2780 and SKOV3 cells in a concentration-time-dependent manner and significantly suppressed the development of tumors in nude mice. CHE elevated the level of oxidative stress in tumor cells, prompted cell cycle halt in the S phase, and increased their mitochondrial membrane potential. Western blotting results demonstrated that CHE could modulate the expression of proteins associated with apoptotic and ferroptosis processes in A2780 and SKOV3 cells. Nrf2 was verified to be an upstream key target mediating the inhibitory impact of CHE on ovarian cancer cells. In summary, CHE exerts its anti-cancer effects on ovarian cancer by modulating Nrf2, inhibiting cellular proliferation, and promoting apoptosis and ferroptosis.

Hepatocellular carcinoma (HCC) is the third most common cancer worldwide, widely prevalent across many countries, and poses a serious threat to human health. With changes in its epidemiology, the incidence of HCC is expected to continue rising. As a class of organic molecules widely distributed in nature, quinone compounds possess notable antioxidant, antibacterial, and antitumor properties. This article selects several quinone compounds that have shown notable research progress in recent years and artificially categorizes them into “plant-derived quinone compounds” and “non-plant-derived quinone compounds.” We then provide a detailed review of the research findings regarding HCC in vitro and in vivo experiments and clinical trials, including their potential toxic side effects. Additionally, based on the varying toxicity reduction of several selected plant-derived quinones when combined with doxorubicin, we further hypothesize that these plant-derived quinone compounds may also exert detoxifying effects on other non-plant-derived quinones discussed in this article. In summary, quinone compounds still hold significant research value and development potential in the fight against HCC. At the same time, we hope our review will provide valuable insights and inspiration for future research in this field.

Sirtuin-3 (SIRT3) is a mitochondrial deacetylase highly expressed in the nervous system, known to regulate mitochondrial homeostasis, energy metabolism, neuroinflammation, apoptosis, and oxidative stress, suggesting its potential neuroprotective role in central nervous system (CNS) disorders. Recent studies indicated that SIRT3 improves neuronal survival by reducing oxidative damage, alleviating neuroinflammation, and modulating autophagy. Therefore, it is imperative to conduct more in-depth and extensive investigations into the mechanisms underlying SIRT3 in central nervous system disorders. This review summarized current research advances on SIRT3, including its fundamental molecular structure, key downstream targets, and mechanisms of action in certain CNS diseases. It further analyzed the potential pharmacological mechanisms of several SIRT3 agonists and explored their therapeutic value in improving CNS disorders. Based on existing evidence, SIRT3 emerges as a promising therapeutic target, offering novel strategies for treating neurological diseases.

Cisplatin resistance significantly limits the efficacy of chemotherapy in non-small cell lung cancer, necessitating the development of new strategies to overcome this barrier. This in vitro study aimed to elucidate the mechanism by which β-Ele reverses cisplatin resistance in lung adenocarcinoma cells via the LINC00511-mediated glycolysis and Wnt/β-catenin signaling pathways. The cisplatin-resistant human lung adenocarcinoma cell line (A549/DDP), with either LINC00511 overexpression or knockdown, was established through plasmid transfection. The transfection efficiency was evaluated using Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR) to detect LINC00511 expression levels. Assessment via the 5-ethynyl-2'-deoxyuridine (EdU) assay indicated significant β-Ele-mediated inhibition of A549/DDP cell proliferation. Further RNA-seq analysis revealed that the inhibitory effect of β-Elemene on cisplatin resistance was closely associated with the interference of cellular glycolysis and the suppression of Wnt/β-catenin signaling pathway activation. Western blot analysis of key proteins, including glucose transporter 1 (GLUT1), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), β-catenin, and glycogen synthase kinase 3β (GSK-3β), showed that β-Elemene reversed cisplatin resistance by inhibiting aerobic glycolysis and blocking the activation of the Wnt/β-catenin signaling pathway through downregulation of LINC00511. Collectively, these results demonstrate that β-Elemene overcomes cisplatin resistance in lung cancer by targeting LINC00511 and its associated aerobic glycolysis/Wnt/β-catenin pathway. This establishes a theoretical framework for future preclinical and clinical investigations while revealing potential therapeutic targets.

Cisplatin resistance significantly limits the efficacy of chemotherapy in non-small cell lung cancer, necessitating the development of new strategies to overcome this barrier. This in vitro study aimed to elucidate the mechanism by which β-Ele reverses cisplatin resistance in lung adenocarcinoma cells via the LINC00511-mediated glycolysis and Wnt/β-catenin signaling pathways. The cisplatin-resistant human lung adenocarcinoma cell line (A549/DDP), with either LINC00511 overexpression or knockdown, was established through plasmid transfection. The transfection efficiency was evaluated using Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR) to detect LINC00511 expression levels. Assessment via the 5-ethynyl-2'-deoxyuridine (EdU) assay indicated significant β-Ele-mediated inhibition of A549/DDP cell proliferation. Further RNA-seq analysis revealed that the inhibitory effect of β-Elemene on cisplatin resistance was closely associated with the interference of cellular glycolysis and the suppression of Wnt/β-catenin signaling pathway activation. Western blot analysis of key proteins, including glucose transporter 1 (GLUT1), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), β-catenin, and glycogen synthase kinase 3β (GSK-3β), showed that β-Elemene reversed cisplatin resistance by inhibiting aerobic glycolysis and blocking the activation of the Wnt/β-catenin signaling pathway through downregulation of LINC00511. Collectively, these results demonstrate that β-Elemene overcomes cisplatin resistance in lung cancer by targeting LINC00511 and its associated aerobic glycolysis/Wnt/β-catenin pathway. This establishes a theoretical framework for future preclinical and clinical investigations while revealing potential therapeutic targets.