Estradiol reduces CCL(4)-induced hepatic fibrosis in rats. The antifibrogenic role of estrogen in the liver may be one reason for the sex associated differences in the progression from hepatic fibrosis to cirrhosis.

No abstract

The increase in hepatic ER and mRNA expression may be part of the molecular mechanisms underlying the suppressive effect of estradiol on liver fibrosis induced by CCl4 administration.

COX-2 expression might correlate with the occurance and advancement of gastric carcinoma and is involved in tumor angiogenesis in gastric carcinoma. It is likely that COX-2 by inducing angiogenesis can be one of mechanisms which promotes invasion and metastasis of gastric carcinoma. It may become a new therapeutic target for anti-angiogenesis.

Recently, long non-coding RNA (lncRNA) FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) has been recognized to function as an oncogene in several human tumors, and FOXD2-AS1 dysregulation has been closely associated with carcinogenesis and tumor progression. Nevertheless, the correlation between the aberrant expression of FOXD2-AS1 and the prognosis of hepatocellular carcinoma (HCC) has not yet been elucidated. In the present study, FOXD2-AS1 was found to be overexpressed in HCC tissues, and FOXD2-AS1 overexpression resulted in significantly shortened patient survival. FOXD2-AS1 overexpression enhanced the viability and metastasis of HCC cells in vitro and in vivo, as revealed by MTT, wound healing and cell migration assays. In addition, mechanistic studies revealed that FOXD2-AS1 upregulated the expression of the miR-206 target gene annexin A2 (ANXA2) by acting as a miR-206 sponge. In summary, FOXD2-AS1 was concluded to function as an oncogene in HCC and to upregulate ANXA2 expression in part by 'sponging' miR-206.