{"title":"蜂王浆和阿霉素通过胸腺裸鼠STAT3/FOXM1/ATG7信号通路抑制肺癌异种移植模型中的肿瘤细胞:生化、免疫组织化学和分子方法","authors":"Tianying Du, Wanjun Wang, Rui Zhang","doi":"10.1093/toxres/tfaf042","DOIUrl":null,"url":null,"abstract":"<p><p>Royal Jelly (RJ), a traditional medicinal compound with tumor-suppressive properties, was investigated for its antitumor effects on non-small cell lung cancer (NSCLC) using a mouse xenograft model. Fifty athymic nude mice were divided into five groups: a control group, an untreated NSCLC group, a doxorubicin (DOX)-treated group, an RJ-treated group, and a combined RJ + DOX treatment group. RJ was administered at 200 mg/kg/day by gavage, while DOX was given intraperitoneally at 80 mg/kg on days 10, 20, and 30. Tumor size, volume, and weight were monitored, and Kaplan-Meier analysis assessed survival. Biochemical and histopathological analyses showed that RJ modulated oxidative stress markers, reduced inflammation (IL-6, TNF-α, IL-8, interferon-γ), and inhibited tumor growth. RJ downregulated STAT3/FOXM1/ATG7 signaling pathways involved in tumor cell survival, proliferation, and metastasis. Additionally, RJ promoted mitochondrial apoptosis through increased p53 expression and reduced angiogenesis by suppressing VEGF. Immunohistochemistry revealed decreased Ki-67 expression, indicating reduced tumor cell proliferation. Molecular analyses confirmed RJ's role in modulating key apoptosis and angiogenesis pathways. When combined with DOX, RJ enhanced therapeutic efficacy, suggesting a synergistic effect. These findings highlight RJ's potential as a therapeutic agent targeting STAT3 and related pathways in NSCLC treatment, offering a promising complementary approach to conventional chemotherapy.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf042"},"PeriodicalIF":2.2000,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11950672/pdf/","citationCount":"0","resultStr":"{\"title\":\"Royal jelly and doxorubicin suppressed tumor cells in the xenograft model of lung cancer via the STAT3/FOXM1/ATG7 signaling pathways in athymic nude mice: a biochemical, immunohistochemically and molecular approach.\",\"authors\":\"Tianying Du, Wanjun Wang, Rui Zhang\",\"doi\":\"10.1093/toxres/tfaf042\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Royal Jelly (RJ), a traditional medicinal compound with tumor-suppressive properties, was investigated for its antitumor effects on non-small cell lung cancer (NSCLC) using a mouse xenograft model. Fifty athymic nude mice were divided into five groups: a control group, an untreated NSCLC group, a doxorubicin (DOX)-treated group, an RJ-treated group, and a combined RJ + DOX treatment group. RJ was administered at 200 mg/kg/day by gavage, while DOX was given intraperitoneally at 80 mg/kg on days 10, 20, and 30. Tumor size, volume, and weight were monitored, and Kaplan-Meier analysis assessed survival. Biochemical and histopathological analyses showed that RJ modulated oxidative stress markers, reduced inflammation (IL-6, TNF-α, IL-8, interferon-γ), and inhibited tumor growth. RJ downregulated STAT3/FOXM1/ATG7 signaling pathways involved in tumor cell survival, proliferation, and metastasis. Additionally, RJ promoted mitochondrial apoptosis through increased p53 expression and reduced angiogenesis by suppressing VEGF. Immunohistochemistry revealed decreased Ki-67 expression, indicating reduced tumor cell proliferation. Molecular analyses confirmed RJ's role in modulating key apoptosis and angiogenesis pathways. When combined with DOX, RJ enhanced therapeutic efficacy, suggesting a synergistic effect. These findings highlight RJ's potential as a therapeutic agent targeting STAT3 and related pathways in NSCLC treatment, offering a promising complementary approach to conventional chemotherapy.</p>\",\"PeriodicalId\":105,\"journal\":{\"name\":\"Toxicology Research\",\"volume\":\"14 2\",\"pages\":\"tfaf042\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2025-03-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11950672/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/toxres/tfaf042\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfaf042","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
Royal jelly and doxorubicin suppressed tumor cells in the xenograft model of lung cancer via the STAT3/FOXM1/ATG7 signaling pathways in athymic nude mice: a biochemical, immunohistochemically and molecular approach.
Royal Jelly (RJ), a traditional medicinal compound with tumor-suppressive properties, was investigated for its antitumor effects on non-small cell lung cancer (NSCLC) using a mouse xenograft model. Fifty athymic nude mice were divided into five groups: a control group, an untreated NSCLC group, a doxorubicin (DOX)-treated group, an RJ-treated group, and a combined RJ + DOX treatment group. RJ was administered at 200 mg/kg/day by gavage, while DOX was given intraperitoneally at 80 mg/kg on days 10, 20, and 30. Tumor size, volume, and weight were monitored, and Kaplan-Meier analysis assessed survival. Biochemical and histopathological analyses showed that RJ modulated oxidative stress markers, reduced inflammation (IL-6, TNF-α, IL-8, interferon-γ), and inhibited tumor growth. RJ downregulated STAT3/FOXM1/ATG7 signaling pathways involved in tumor cell survival, proliferation, and metastasis. Additionally, RJ promoted mitochondrial apoptosis through increased p53 expression and reduced angiogenesis by suppressing VEGF. Immunohistochemistry revealed decreased Ki-67 expression, indicating reduced tumor cell proliferation. Molecular analyses confirmed RJ's role in modulating key apoptosis and angiogenesis pathways. When combined with DOX, RJ enhanced therapeutic efficacy, suggesting a synergistic effect. These findings highlight RJ's potential as a therapeutic agent targeting STAT3 and related pathways in NSCLC treatment, offering a promising complementary approach to conventional chemotherapy.