This study was aimed to explore the anti-tumor functions of Ginseng on the human lung cancer cells A549, through investigating the effects of water extract of Ginseng(WEG), Ginseng polysaccharides(GPS)and Ginseng total saponins(GTS)on cell proliferation, cell migration and cytoskeleton of A549 cells. Using A549 cells as target cells, the TAMs model in vitro was established from THP-1. MTT method was used to observe the effects of different concentrations of WEG, GPS, GTS on A549 cells in co-culture system of TAMs with A549 cells. The cell migration of A549 cells was assayed by real-time cell analysis(RTCA). The cytoskeleton of A549 cells was detected by high content screening(HCS). It showed that in the co-culture system, WEG inhibited the proliferation, migration, and the area of cytoskeleton on A549 cells significantly(P< 0. 01). GPS inhibited A549 cell migration and the area of cytoskeleton(P < 0. 01)in co-culture system, but it showed no significant effect on the proliferation of A549 cells. Moreover, GTS can significant inhibit the proliferation of A549 cells(P< 0. 01), and the effect on the cell migration and the area of cytoskeleton was in conspicuous in the co-culture system. It was found that the two main components of ginseng showed different functions by the comparison of WEG, GPS, GTS in TAMs co-culture system. Results indicate that the antitumor effects of ginseng may be due to its multi-component regulation in the tumor microenvironment.

Objective To investigate the effect of long non-coding RNA(lncRNA)lung cancer-related transcript 1(LUCAT1)on the pathogenesis of intrauterine adhesion by regulating the expression of amphiregulin(AREG),to provide a new molecular target for the prevention and treatment of intrauterine adhesions.Methods Real-time quantitative polymerase chain reaction(RTqPCR)was used to determine the mRNA expression levels of lncRNA LUCAT1,fibrotic markers of α-smooth muscle actin(α-SMA)and collagen type Ⅰ alpha 1 chain protein(COL1A1)in samples of intrauterine adhesion tissue and endometrial stromal cell treated with transforming growth factor-β1.Western blot was used to determine the protein expression levels of AREG,α-SMA,COL1A1.Then,si-LUCAT1,pcDNA LUCAT1,si-AREG were transfected into ESC and RT-qPCR was used to detect the mRNA expression levels of lncRNA LUC-AT1 and AREG.Next,si-LUCAT1 and pcDNA LUCAT1 were transfected into ESC and treated these cells with TGF-β1 for 48h,re-spectively.Western blot was used to further detect the protein expression levels of AREG,α-SMA and COL1A1,and cell proliferation and apoptosis were detected by cell proliferation assay and cell apoptosis assay.Results The expression levels of lncRNA LUC AT1,AR-EG and fibrosis markers α-SMA and COL1A1 were upregulated in endometrial tissues from patients with intrauterine adhesion and in ESC that had been treated with TGF-β1.AREG changed with the change of lncRNA LUCAT1,and the expression of lncRNA LUC-AT1did not change significantly after downregulation of AREG,and AREG was positively regulated by lncRNA LUCAT1.During the process of the transformation of ESC into fibroblasts,si-LUCAT1 significantly inhibited the protein expression levels of AREG,α-SMA and COL1A1(P＜0.01),significantly reduced cell proliferation and significantly induced cell apoptosis,the difference was statistically significant(P＜0.001).pcDNA LUCAT1 significantly induced the protein expression levels of AREG,α-SMA and COL1A1,and the difference was statistically significant(P＜0.01).Conclusion LncRNA LUCAT1 promotes the pathogenesis of intrauterine adhesion by up-regulating the expression of AREG.LncRNA LUCAT1/AREG axis may provide novel molecular target for the prevention and treat-ment of intrauterine adhesion.