ABSTRACT
Objective To discuss the effect of breast cancer anti-estrogen resistance 1(BCAR1) knockdown on the expression of P38 and p-P38 in lung cancer cell line A549. Methods A549 cells (control group), A549 cells with RNAi letiviral vector of BCAR1 (interference group) and A549 cells with negative control letiviral vector (negative group) were cultured. Western blot was used to detect the expression of P38 and p-P38. The prolifera-tion,cell cycle,migration and invasion were measured by colony formation assay,flow cytometer,transwell experi-ment and scratch adhesion test,respectively. Results p-P38 expression in interference group cells was significant-ly lower than that in other two group cells(P<0.05).G1phase of interference group cells was significantly increas-ing than that in other two group cells(P<0.05).The proliferation,migration and invasion of interference group cells were all significantly suppressed as compared with that of other two group cells(P<0.05). Conclusions BCAR1 knockdown decreases p-P38 expression and inhibits proliferation,migration and invasion of A549 cells.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the proliferation-inhibiting and apoptosis-inducing effects of ursolic acid (UA) and oleanolic acid (OA) on multi-drug resistance (MDR) cancer cells in vitro.</p><p><b>METHODS</b>UA and OA in different concentrations (0-100 μmol/L) were added separately to cultures of different cancer cell lines, including the human colon cancer cell lines SW480 and SW620, human acute myelocytic leukemia cancer cell lines HL60 and HL60/ADR, human chronic myelogenous leukemia cell lines K562 and K562/ADR, and the human breast cancer cell lines MCF-7 and MCF-7/ADR. Effects of UA and OA on cell proliferation were detected by 3-(4,5-dimethyl-2-thiazole)-2-5-biphenly-tetrazole bromide (MTT) method and effects on cell apoptosis were tested by flow cytometry (FCM) and Western blot at 24, 48, and 72 h after treatment.</p><p><b>RESULTS</b>Both UA and OA showed significant inhibition on parent and MDR cell lines in a time- and concentration-dependent manner; the drug-resistant multiple of them on K562 and K562/ADR as well as on HL60 and HL60/ADR was 1; the effects of UA were better than those of OA in inhibiting cell growth of solid colonic cancer and breast cancer. After SW480 cells were treated by UA at the concentrations of 0-40 μmol/L for 48 h, FCM showed that annexin V (AV) positive cells and hypodiploid peak ratio increased along with the increase in the drug's concentrations; and Western blot found that expressions of Bcl-2, Bcl-xL and survivin decreased in a concentration-dependent manner.</p><p><b>CONCLUSIONS</b>Both UA and OA have antitumor effects on cancer cells with MDR, and the optimal effect is shown by UA on colonic cancer cells. Also, UA shows cell apoptosis-inducing effect on SW480, possibly by way of down-regulating the expressions of apoptosis antagonistic proteins, Bcl-2, Bcl-xL, and survivin.</p>