Yu-Chen S H Yang, Chung-Che Tsai, Yung-Ning Yang, Feng-Cheng Liu, Sheng-Yang Lee, Jen-Chang Yang, Dana R Crawford, Hsien-Chung Chiu, Mei-Chin Lu, Zi-Lin Li, Yi-Chen Chen, Tin-Yi Chu, Jacqueline Whang-Peng, Hung-Yun Lin, Kuan Wang
{"title":"在胆管癌中，Heteronemin通过PI3K/PD - L1信号通路抑制EGF诱导的增殖。","authors":"Yu-Chen S H Yang, Chung-Che Tsai, Yung-Ning Yang, Feng-Cheng Liu, Sheng-Yang Lee, Jen-Chang Yang, Dana R Crawford, Hsien-Chung Chiu, Mei-Chin Lu, Zi-Lin Li, Yi-Chen Chen, Tin-Yi Chu, Jacqueline Whang-Peng, Hung-Yun Lin, Kuan Wang","doi":"10.3892/or.2025.8865","DOIUrl":null,"url":null,"abstract":"<p><p>Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells. It inhibits critical signal transduction pathways promoted by the EGF. In the current study, EGF‑induced signal activation and proliferative effects were investigated in cholangiocarcinoma cells and its molecular targets using qPCR and western blotting analyses. In addition, cell viability assays were performed to assess the growth effects of EGF and heteronemin. Heteronemin reversed the effects of EGF and was further enhanced by blockage of PI3K's activity. In summary, EGF stimulates cholangiocarcinoma cell growth. On the other hand, heteronemin inhibited PI3K activation and PD‑L1 expression to reverse the stimulative effects of EGF‑induced gene expression and proliferation in cholangiocarcinoma cells.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma.\",\"authors\":\"Yu-Chen S H Yang, Chung-Che Tsai, Yung-Ning Yang, Feng-Cheng Liu, Sheng-Yang Lee, Jen-Chang Yang, Dana R Crawford, Hsien-Chung Chiu, Mei-Chin Lu, Zi-Lin Li, Yi-Chen Chen, Tin-Yi Chu, Jacqueline Whang-Peng, Hung-Yun Lin, Kuan Wang\",\"doi\":\"10.3892/or.2025.8865\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells. It inhibits critical signal transduction pathways promoted by the EGF. In the current study, EGF‑induced signal activation and proliferative effects were investigated in cholangiocarcinoma cells and its molecular targets using qPCR and western blotting analyses. In addition, cell viability assays were performed to assess the growth effects of EGF and heteronemin. Heteronemin reversed the effects of EGF and was further enhanced by blockage of PI3K's activity. In summary, EGF stimulates cholangiocarcinoma cell growth. On the other hand, heteronemin inhibited PI3K activation and PD‑L1 expression to reverse the stimulative effects of EGF‑induced gene expression and proliferation in cholangiocarcinoma cells.</p>\",\"PeriodicalId\":19527,\"journal\":{\"name\":\"Oncology reports\",\"volume\":\"53 3\",\"pages\":\"\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2025-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oncology reports\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/or.2025.8865\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/10 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oncology reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/or.2025.8865","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/10 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma.
Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells. It inhibits critical signal transduction pathways promoted by the EGF. In the current study, EGF‑induced signal activation and proliferative effects were investigated in cholangiocarcinoma cells and its molecular targets using qPCR and western blotting analyses. In addition, cell viability assays were performed to assess the growth effects of EGF and heteronemin. Heteronemin reversed the effects of EGF and was further enhanced by blockage of PI3K's activity. In summary, EGF stimulates cholangiocarcinoma cell growth. On the other hand, heteronemin inhibited PI3K activation and PD‑L1 expression to reverse the stimulative effects of EGF‑induced gene expression and proliferation in cholangiocarcinoma cells.
期刊介绍：
Oncology Reports is a monthly, peer-reviewed journal devoted to the publication of high quality original studies and reviews concerning a broad and comprehensive view of fundamental and applied research in oncology, focusing on carcinogenesis, metastasis and epidemiology.
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