{"title":"二甲双胍通过IGF-1R/miR-610/FEN1通路使骨肉瘤对化疗敏感。","authors":"Suwei Dong, Yanbin Xiao, Ziqiang Zhu, Xiang Ma, Zhuohui Peng, Jianping Kang, Jianqiang Wang, Yunqing Wang, Zhen Li","doi":"10.4081/ejh.2023.3612","DOIUrl":null,"url":null,"abstract":"<p><p>Metformin can enhance cancer cell chemosensitivity to anticancer drugs. IGF-1R is involved in cancer chemoresistance. The current study aimed to elucidate the role of metformin in osteosarcoma (OS) cell chemosensitivity modulation and identify its underlying mechanism in IGF-1R/miR-610/FEN1 signalling. IGF-1R, miR-610, and FEN1 were aberrantly expressed in OS and participated in apoptosis modulation; this effect was abated by metformin treatment. Luciferase reporter assays confirmed that FEN1 is a direct target of miR-610. Moreover, metformin treatment decreased IGF-1R and FEN1 but elevated miR-610 expression. Metformin sensitised OS cells to cytotoxic agents, while FEN1 overexpression partly compromised metformin's sensitising effects. Furthermore, metformin was observed to enhance adriamycin's effects in a murine xenograft model. Metformin enhanced OS cell sensitivity to cytotoxic agents via the IGF-1R/miR-610/FEN1 signalling axis, highlighting its potential as an adjuvant during chemotherapy.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/47/7c/ejh-67-2-3612.PMC10230554.pdf","citationCount":"0","resultStr":"{\"title\":\"Metformin sensitises osteosarcoma to chemotherapy <em>via</em> the IGF-1R/miR-610/FEN1 pathway.\",\"authors\":\"Suwei Dong, Yanbin Xiao, Ziqiang Zhu, Xiang Ma, Zhuohui Peng, Jianping Kang, Jianqiang Wang, Yunqing Wang, Zhen Li\",\"doi\":\"10.4081/ejh.2023.3612\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Metformin can enhance cancer cell chemosensitivity to anticancer drugs. IGF-1R is involved in cancer chemoresistance. The current study aimed to elucidate the role of metformin in osteosarcoma (OS) cell chemosensitivity modulation and identify its underlying mechanism in IGF-1R/miR-610/FEN1 signalling. IGF-1R, miR-610, and FEN1 were aberrantly expressed in OS and participated in apoptosis modulation; this effect was abated by metformin treatment. Luciferase reporter assays confirmed that FEN1 is a direct target of miR-610. Moreover, metformin treatment decreased IGF-1R and FEN1 but elevated miR-610 expression. Metformin sensitised OS cells to cytotoxic agents, while FEN1 overexpression partly compromised metformin's sensitising effects. Furthermore, metformin was observed to enhance adriamycin's effects in a murine xenograft model. Metformin enhanced OS cell sensitivity to cytotoxic agents via the IGF-1R/miR-610/FEN1 signalling axis, highlighting its potential as an adjuvant during chemotherapy.</p>\",\"PeriodicalId\":50487,\"journal\":{\"name\":\"European Journal of Histochemistry\",\"volume\":\"67 2\",\"pages\":\"\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2023-05-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/47/7c/ejh-67-2-3612.PMC10230554.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European Journal of Histochemistry\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.4081/ejh.2023.3612\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Histochemistry","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.4081/ejh.2023.3612","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Metformin sensitises osteosarcoma to chemotherapy via the IGF-1R/miR-610/FEN1 pathway.
Metformin can enhance cancer cell chemosensitivity to anticancer drugs. IGF-1R is involved in cancer chemoresistance. The current study aimed to elucidate the role of metformin in osteosarcoma (OS) cell chemosensitivity modulation and identify its underlying mechanism in IGF-1R/miR-610/FEN1 signalling. IGF-1R, miR-610, and FEN1 were aberrantly expressed in OS and participated in apoptosis modulation; this effect was abated by metformin treatment. Luciferase reporter assays confirmed that FEN1 is a direct target of miR-610. Moreover, metformin treatment decreased IGF-1R and FEN1 but elevated miR-610 expression. Metformin sensitised OS cells to cytotoxic agents, while FEN1 overexpression partly compromised metformin's sensitising effects. Furthermore, metformin was observed to enhance adriamycin's effects in a murine xenograft model. Metformin enhanced OS cell sensitivity to cytotoxic agents via the IGF-1R/miR-610/FEN1 signalling axis, highlighting its potential as an adjuvant during chemotherapy.
期刊介绍：
The Journal publishes original papers concerning investigations by histochemical and immunohistochemical methods, and performed with the aid of light, super-resolution and electron microscopy, cytometry and imaging techniques. Coverage extends to:
functional cell and tissue biology in animals and plants;
cell differentiation and death;
cell-cell interaction and molecular trafficking;
biology of cell development and senescence;
nerve and muscle cell biology;
cellular basis of diseases.
The histochemical approach is nowadays essentially aimed at locating molecules in the very place where they exert their biological roles, and at describing dynamically specific chemical activities in living cells. Basic research on cell functional organization is essential for understanding the mechanisms underlying major biological processes such as differentiation, the control of tissue homeostasis, and the regulation of normal and tumor cell growth. Even more than in the past, the European Journal of Histochemistry, as a journal of functional cytology, represents the venue where cell scientists may present and discuss their original results, technical improvements and theories.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
