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Journal of Translational Medicine

, 12:93

Cancer microenvironment


Hepatocellular carcinoma HCC is one of the most common malignancies worldwide and accounts for the third-leading cause of cancer-related deaths. Over the past decades, advances have been made in the field of surgery, but effective treatment of HCC is lacking. Due to a marked male predominance in morbidity and mortality in HCC patients, it has long been considered that sex hormones play a role in HCC development. Recently estrogen has been proven to exert protective effects against HCC through IL-6 restrictions, STAT3 inactivation and tumour-associated macrophage inhibition. While IL-6-dependent STAT3 activation is considered a key event in inflammation-induced liver cancer, the anti-inflammation effect of estrogen is well documented. The roles of the estrogen receptor and aromatase and interactions between microRNAs and estrogen in HCC have been investigated. In this review, we present a novel model to elucidate the mechanism of estrogen-mediated inhibition of HCC development through an anti-inflammation effect and provide new insights into the roles of estrogen in liver disease.

KeywordsEstrogen Estrogen receptor Hepatocellular carcinoma Inflammation AbbreviationsHCCHepatocellular carcinoma

EREstrogen receptor

OCPsOral contraceptives

EREEstrogen response element

wtER-αWild type ER-α

vER-αVariant ER-α


HBxHepatitis B virus X protein

HBS-AgHepatitis B surface antigen

LINE-1Long interspersed nuclear element-1

KCsKupffer cells


FoxaForkhead box A

TAMsTumour-associated macrophages

STATSignal transducer and activator of transcription

SOCSSuppressor of cytokine signalling

PTPROprotein tyrosine phosphatase receptor type O.

Electronic supplementary materialThe online version of this article doi:10.1186-1479-5876-12-93 contains supplementary material, which is available to authorized users.

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Author: Liang Shi - Yili Feng - Hui Lin - Rui Ma - Xiujun Cai


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