ABSTRACT
Long non-coding RNA(lncRNA)is a class of RNAs with a number of nucleotides greater than 200,no specific open reading frame and no protein coding. LncRNA could have a sig-nificant influence on the regulation of gene expression during cell growth,and also play a potential role in the development,pro-gression and resistance of tumors. Consequently,it becomes a new tumor research hot spot after miRNA. Many studies have shown that aberrant expression of lncRNA may lead to anti-tumor drug resistance. Furthermore,this resistance is not only derived from individual differences in patients,but also from genetic and epigenetic differences in the tumor. In this paper,we summarize the recent advances in lncRNAs associated with drug resistance that may help overcome drug resistance,so as to improve and develop new therapeutic strategies.
ABSTRACT
Aim To investigate the anticancer activity and the mechanism of the apoptosis induced by Ama-ranthus spinosus L. extract ( ASE ) in human hepatic carcinoma cell line HepG2 . Methods Alamar blue assay was used for detecting the influence of ASE on the proliferation of the cancer cells. The morphological changes of cells were observed under inverted micro-scope and Hoechst 33258 stainning. The apoptosis of HepG2 cells was detected by flow cytometry. Western blot and caspase-3 activity kit were used to detect the protein expression in HepG2 cells. The specific inhibi-tor of caspase-9 and caspase-3 ( Z-LEHD-FMK and Ac-DEVD-CHO) was used to validate the signal transduc-tion pathyway. Results The results indicated that the cell proliferation was inhibited by ASE,especicially the HepG2 cells. The HepG2 cells showed obvious apop-totic characteristics. Flow cytometry analysis further validated the apoptosis of HepG2 cells. The expression of Bcl-2 and survivin was downreagulated in HepG2 cells treated with ASE, and Bax, caspase-9, caspase-3, Apaf-1 and PARP were upregualted. Besides, the caspase-3 activity was also increased. Z-LEHD-FMK and Ac-DEVD-CHO significantly increased the cell vi-abilty of HepG2 cells induced by ASE. Conclusion These results confirm that ASE induces the apoptosis of HepG2 through mitochondria-mediated pathway.