Long non-coding RNAs (lncRNAs) are involved in the development and progression of a variety of diseases. However, the role of the lncRNA HLA complex group 11 (HCG11) in non-small cell lung cancer (NSCLC) remains unclear. The present study showed that the expression levels of HCG11 were reduced in tumor tissues compared with adjacent normal tissues, and similar results were obtained in experiments using lung cancer cell lines. Additionally, patients with high HCG11 expression had an increased survival rate compared with patients with low HCG11 expression. Further studies have shown that overexpression of HCG11 inhibited NSCLC cell proliferation in vitro and in vivo . Interestingly, it was observed that HCG11 expression was negatively associated with the expression levels of oncogenic microRNA-875 (miR-875) in patient specimens. Specifically, HCG11 served as a sponge of miR-875. Notably, it was determined that special AT-rich sequence-binding protein 2 (SATB2) was a direct target gene of miR-875, and overexpression of miR-875 largely abrogated the effects of HCG11 in NSCLC cells. In conclusion, HCG11 was shown to suppress the malignant properties of NSCLC cells by targeting a miR-875/SATB2 axis, and may therefore be a promising target for the treatment of NSCLC.

Copper (Cu) is an essential metal required for many physiological processes and biological reactions. Liver is the main organ of metabolism of Cu, and is also the site where synthesis of some metalloproteins. The purpose of this study is to explore the effects of Cu deficiency on the liver, and to evaluate the changes in liver oxidative stress levels to reveal its possible impact mechanisms. Mice were feed to a nutritional Cu-deficiency diet from weaning and injected with copper sulphate (CuSO4) intraperitoneally to correct Cu deficiency. Cu deficiency resulted in reduced liver index, liver histological alteration and oxidative stress, decreased the contents of Cu and ALB, elevated ALT and AST concentrations in serum together with decreased mRNA and protein expressions of Nrf2 pathway related molecules (Nrf2, HO-1, NQO1), increased mRNA and protein expressions of Keap1. However, the supplement of CuSO4 significantly ameliorated the changes mentioned above. Our results indicate that Cu deficiency can cause hepatic damage in mice is associated with the activation of oxidative stress and inhibition of Nrf2 pathway.

Copper (Cu) is an essential metal required for many physiological processes and biological reactions.Liver is the main organ of metabolism of Cu, and is also the site where synthesis of some metalloproteins. The purpose of this study is to explore the effects of Cu de ciency on the liver, and to evaluate the changes in liver oxidative stress levels to reveal its possible impact mechanisms. Mice were feed to a nutritional Cu-de ciency diet from weaning and injected with copper sulphate (CuSO 4 ) intraperitoneally to correct Cu de ciency. Cu de ciency resulted in reduced liver index, liver histological alteration and oxidative stress, decreased the contents of Cu and ALB, elevated ALT and AST concentrations in serum together with decreased mRNA and protein expressions of Nrf 2 pathway related molecules (Nrf2, HO-1, NQO1), increased mRNA and protein expressions of Keap1. However, the supplement of CuSO 4 signi cantly ameliorated the changes mentioned above. Our results indicate that Cu de ciency can cause hepatic damage in mice is associated with the activation of oxidative stress and inhibition of Nrf 2 pathway.