Arteasunate Inhibit the Proliferation of Skin Cancer Cell Line A431 ...

Abstract

Cancer is the most primary etiological factor in multitude fatal diseases. With the environmental disruption, aerial pollution, ultraviolet radiation, abusing of drugs and cosmetics, increasing the aging etc., incidence of carcinoma cutaneum becomes much higher. even being one of the most common malignant tumor; especially,homo-latitude territory, the incidence is higher than any other malignant tumors. In one word, cutaneous cancer is seriously hazarding health. At present, the regular therapeutics have some defects, including low effective and high toxicity. Therefore, finding the effective method of curing cutaneous cancer becomes more and more urgent.Artemisinin and derivates are famous as high performance of anti-malaria. Lately, the effection of anticancer was applied. Arteasunate(ART) is water-solubility derived of Artemisinin. It was reported that ART showing the obviouse growth inhibition of HL60, KB. OV3, BGC823, Hela, SGC7901, A549, KCC853 and GLC-82. The mechanism of inhibition was multiply, including inducing apoptosis, arresting cell cycle, immuno-modulation and reversing drug fast, but had certified potentia of idio-impairment for cancer cell. However, the mechanism of ART affecting cutaneous cancer was unknow. Based on low toxicity, high performance, we tested apoptosis and cell cycle, A431 treated with ART, ART combining with DFOM or FeSO4. Fllowing, the mechanism studying to explain the effct of ido- inhibition , and to provided the new evidence experiment of clinic test.The result shew: ART can significant inhibit growth of SW480,HepG2?A431, and the effect relied on time and dose of action; we compared the growth inhibition of DDP to the effction of ART for HaCaT, the result shew that ART is lew toxicant, compared with DDP at the same dosage, suggesting that ART was low side effect, may potent appliment in clinic therapy.The results of apoptosis: A431 ce1l were exposured to ART, appeared typical apoptosis features, including chromatin condensation and apoptotic bodies;and the rate of apoptosis(19.87?3.2)% and death(17.5?0.50)% increasing,[the apoptosis of Cntrol(2.57?1.93)%, the death of Cntrol (2.1?1.22) % ],accompanying with up-regulation of Bax/Bcl-2(1.06 to 2.91). And DFOM , Fe2+ blocking agent , could partly blocked the inhibition of ART, including decreasing the quantity of A431 which presebting apoptosis features, the rate of apoptosi(s7.37?1.8%)and death(13.5?0.9)% decreasing, down-regulation of Bax/Bcl-2(2.91 to 1.56), the FeSO4 enforced the inhibition of ART, suggesting Fe is possibly contribution to inducing apoptosis by ART.The test of cycle shew: to control, ART arrested significantly the A431 in S state; To deeply study suggested that ART could down-regulate Cyclin-A, E, B1; up-regulate of P21, Cyclin-D1 and Cdk-4; and down-regulattion of Cyclin-E was significantly. The changes of cycle regulate-ralate protein was may responsibility to S state arresting.With all the results, we could include that ART can specialy inhibite the growth of carcinoma cutaneum cell line A431, the inhibition including induing apoptosis, promoting death and arresting cell cycle; Fe2+ may be contribution to apotosis and death, the arresting cell cyle should be ralted with cycle-regulation proteins.

Source: http://www.res-medical.com/oncology/63821

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