Payel Guha, Koushik Sen, Piyali Chowdhury, Dilip Mukherjee
{"title":"雌激素受体作为子宫内膜癌的潜在治疗靶点。","authors":"Payel Guha, Koushik Sen, Piyali Chowdhury, Dilip Mukherjee","doi":"10.1080/10799893.2023.2187643","DOIUrl":null,"url":null,"abstract":"<p><p>Endometrial cancer (EC) is one of the most common gynecological carcinomas in both developed and developing countries. Majority of the gynecological malignancies are hormonally driven where estrogen signaling acts as an oncogenic signal. Estrogen's effects are mediated <i>via</i> classical nuclear estrogen receptors; estrogen receptor alpha and beta (ERα and ERβ) and a trans-membrane G protein-coupled estrogen receptor (GPR30 and GPER). ERs and GPER through ligand binding triggers multiple downstream signaling pathways causing cell cycle regulation, cell differentiation, migration, and apoptosis in various tissues including endometrium. Although the molecular aspect of estrogen function in ER-mediated signaling is now partly understood, the same is not true for GPER-mediated signaling in endometrial malignancies. Understanding the physiological roles of ERα and GPER in EC biology therefore leads to the identification of some novel therapeutic targets. Here we review the effect of estrogen signaling through ERα-and GPER in EC, major types, and some affordable treatment approaches for endometrial tumor patients which has interesting implications in understanding uterine cancer progression.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"43 1","pages":"19-26"},"PeriodicalIF":2.6000,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Estrogen receptors as potential therapeutic target in endometrial cancer.\",\"authors\":\"Payel Guha, Koushik Sen, Piyali Chowdhury, Dilip Mukherjee\",\"doi\":\"10.1080/10799893.2023.2187643\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Endometrial cancer (EC) is one of the most common gynecological carcinomas in both developed and developing countries. Majority of the gynecological malignancies are hormonally driven where estrogen signaling acts as an oncogenic signal. Estrogen's effects are mediated <i>via</i> classical nuclear estrogen receptors; estrogen receptor alpha and beta (ERα and ERβ) and a trans-membrane G protein-coupled estrogen receptor (GPR30 and GPER). ERs and GPER through ligand binding triggers multiple downstream signaling pathways causing cell cycle regulation, cell differentiation, migration, and apoptosis in various tissues including endometrium. Although the molecular aspect of estrogen function in ER-mediated signaling is now partly understood, the same is not true for GPER-mediated signaling in endometrial malignancies. Understanding the physiological roles of ERα and GPER in EC biology therefore leads to the identification of some novel therapeutic targets. Here we review the effect of estrogen signaling through ERα-and GPER in EC, major types, and some affordable treatment approaches for endometrial tumor patients which has interesting implications in understanding uterine cancer progression.</p>\",\"PeriodicalId\":16962,\"journal\":{\"name\":\"Journal of Receptors and Signal Transduction\",\"volume\":\"43 1\",\"pages\":\"19-26\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2023-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Receptors and Signal Transduction\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/10799893.2023.2187643\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Receptors and Signal Transduction","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/10799893.2023.2187643","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Estrogen receptors as potential therapeutic target in endometrial cancer.
Endometrial cancer (EC) is one of the most common gynecological carcinomas in both developed and developing countries. Majority of the gynecological malignancies are hormonally driven where estrogen signaling acts as an oncogenic signal. Estrogen's effects are mediated via classical nuclear estrogen receptors; estrogen receptor alpha and beta (ERα and ERβ) and a trans-membrane G protein-coupled estrogen receptor (GPR30 and GPER). ERs and GPER through ligand binding triggers multiple downstream signaling pathways causing cell cycle regulation, cell differentiation, migration, and apoptosis in various tissues including endometrium. Although the molecular aspect of estrogen function in ER-mediated signaling is now partly understood, the same is not true for GPER-mediated signaling in endometrial malignancies. Understanding the physiological roles of ERα and GPER in EC biology therefore leads to the identification of some novel therapeutic targets. Here we review the effect of estrogen signaling through ERα-and GPER in EC, major types, and some affordable treatment approaches for endometrial tumor patients which has interesting implications in understanding uterine cancer progression.
期刊介绍:
Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services:
BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.