Article(id=1218551207950471750, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1218551204993487072, articleNumber=null, orderNo=null, doi=10.16438/j.0513-4870.2018-0530, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1528128000000, receivedDateStr=2018-06-05, revisedDate=1529856000000, revisedDateStr=2018-06-25, acceptedDate=null, acceptedDateStr=null, onlineDate=1768454847562, onlineDateStr=2026-01-15, pubDate=1541952000000, pubDateStr=2018-11-12, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1768454847562, onlineIssueDateStr=2026-01-15, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1768454847562, creator=13701087609, updateTime=1768454847562, updator=13701087609, issue=Issue{id=1218551204993487072, tenantId=1146029695717560320, journalId=1189982191388893191, year='2018', volume='53', issue='11', pageStart='1761', pageEnd='1942', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1768454846857, creator=13701087609, updateTime=1768457167276, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1218560937590702204, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1218551204993487072, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1218560937590702205, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1218551204993487072, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1761, endPage=1769, ext={EN=ArticleExt(id=1218551210211201858, articleId=1218551207950471750, tenantId=1146029695717560320, journalId=1189982191388893191, language=EN, title=Macrophage migration inhibitory factor, a critical link between inflammation and cancer, columnId=1190335348648547107, journalTitle=Acta Pharmaceutica Sinica, columnName=REVIEWS, runingTitle=null, highlight=null, articleAbstract=

Macrophage migration inhibitory factor (MIF) is a classical pro-inflammatory cytokine that plays an important role in the innate and adaptive immune regulation. In recent years, a large number of studies have demonstrated that the expression level of MIF is significantly increased in a variety of tumor tissues and MIF promotes the occurrence and development of tumors. MIF participates in the regulation of tumor growth, metastasis, angiogenesis, as well as induces and maintains the tumor microenvironment. Targeting MIF has been considered as a candidate strategy against cancer. In this review, the structural features, the signaling pathway, the biological functions of MIF are briefly outlined. Moreover, approaches that target MIF in the treatment of cancer are also summarized.

, correspAuthors=Zhuo-wei HU, authorNote=null, correspAuthorsNote=null, copyrightStatement=Copyright ©2018 Acta Pharmaceutica Sinica. All rights reserved., copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, authorCompany=null, fund=null, authors=null, authorsList=Dan-dan ZHOU, Jiao-jiao YU, Fang HUA, Zhuo-wei HU), CN=ArticleExt(id=1218551211712762857, articleId=1218551207950471750, tenantId=1146029695717560320, journalId=1189982191388893191, language=CN, title=巨噬细胞迁移抑制因子, 连接炎症和肿瘤的关键蛋白, columnId=1190335349655180086, journalTitle=药学学报, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

巨噬细胞迁移抑制因子（MIF）是一种经典的促炎因子，参与先天性和适应性免疫应答调节。大量研究显示，MIF在多种肿瘤组织中表达显著增加，促进肿瘤生长、转移、血管新生，并诱导形成促肿瘤免疫微环境。鉴于MIF在肿瘤发生、发展过程中的重要促进作用，靶向MIF被认为是治疗肿瘤的潜在策略。本文对MIF的特性、分布特点、信号通路、在炎症、肿瘤中的生物学功能以及靶向MIF药物开发等方面的最新进展进行综述。

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Macrophage migration inhibitor factor (MIF) signaling pathways. MIF regulates cell function through receptor-mediated and intracellular interactions. MIF interacts with the JAB1 and promotes cell proliferation; MIF forms a complex with CD74 or CD74/ CD44, leading to ERK1/2 activation, which triggers the release of pro-inflammatory cytokines. In the process, the tumor suppressor p53 is down-regulated along with activation of phospholipase A2 (PLA2) and cyclooxygenase 2 (COX2) leads to the inhibition of apoptosis. The PI3K/Akt pathway is also activated, leading to the release of angiogenesis factor such as ICAM-1, VCAM-1, which further contributes to angiogenesis

, figureFileSmall=myQxbNkJHGjS2NTeORrrPA==, figureFileBig=eUjaROm7OxzvUlmzUtbkSA==, tableContent=null), ArticleFig(id=1218970808899256341, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1218551207950471750, language=EN, label=null, caption=null, figureFileSmall=GXB14loKHhMHMOo9wzvIJA==, figureFileBig=LPT2ghRvOuUmMc01knowpw==, tableContent=null), ArticleFig(id=1218970809033474076, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1218551207950471750, language=CN, label=Figure 2, caption=

Strategies for targeted MIF treatment. MIF’s functional activity can be suppressed in many ways. Small molecule inhibitors block the binding of MIF to receptors CD74 or CD74/CD44, and the downstream signal pathway is suppressed, such as p53-dependent apoptosis, ERK1/2 activation and COX-2/PGE-2 production. Some MIF inhibitors can also enter the cell to prevent the protein interaction of MIF. Anti-MIF antibodies can generate similar functionality. HSP90 can stabilize intracellular MIF, so the HSP90 inhibitors can promote MIF degradation

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