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11, 25 dihydroxy vitamin D3, an active metabolite of vitamin­D3 has been reported to inhibit the growth of number neoplasms such as prostate, breast, colorectal, leukemia and skin cancers. Valproic acid, as a potent histone deacetylase inhibitor, also plays an important role in inhibition of proliferation of tumor cells. However, there are no reports so far on the cooperation between valproic acid and vitamin­ D3 for anti-leukemic effect. The goal of the present research was to evaluate whether low doses of vitamin D3 potentiate the toxicity of valproic acid and whether this toxic action is mediated via apoptotic mechanisms. In this study HL-60 cells were treated either with different concentrations of valproic acid and vitamin­ D3 alone and in combination with each other for 24 hours. Cell survival was determined by MTT assay and then Hoechst staining was used to determine the type of death cell. This present study indicates that vitamin ­D3 potentiates the antitumor effects of valproic acid. Also, the results of staining cells showed that valproic acid and vitamin ­D3 induced apoptosis in HL-60 cells. In total, the new combination of valproic acid and vitamin D3 showed synergistic anti-proliferative effect and induced apoptosis on HL-60 cancer cells.
                                                                       

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In this study, the cytotoxic effects of aqueous and ethanolic extracts of Sedum album L. on human stomach cancer cell line (AGS) and breast cancer cell line (MCF-7) were evaluated by MTT, BrdU and TUNEL assays. The results demonstrated that both extracts had antiproliferative and apoptotic effects in a dose-dependent manner. The MTT assay data revealed that the AGS cell underwent more cytotoxicity in comparison with the MCF-7 cell. It also revealed that ethanolic extract was more potent than aqueous extract. The BrdU assay results showed that the proliferation of AGS and MCF-7 cells was reduced to 50% and 43%, respectively, at the highest concentration of the aqueous extract. In addition, the ethanolic extract reduced the proliferation of AGS and MCF-7 cells to 75% and 60%, respectively. The AGS and MCF-7 cells underwent 52% and 12% apoptotic death upon treatment by the ethanolic extract as TUNEL assay showed. The aqueous extract induced 28% and 25% apoptosis in the AGS and MCF-7 cells, respectively. Both inhibition of proliferation and induction of apoptosis are desirable strategies for cancer treatment among researchers. Identification of S. album compounds and analyzing their effects in animal model of cancer can help us with understanding its anti-cancer properties.
 

 

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Lung carcinoma is the second most common type of cancer. Inefficiency of the current treatments and the undesirable side effects of chemotherapy drugs made the know-how of the treatment important. The purpose of this study is to investigate the synergic effect of curcumin and Cisplatin in comparison with the sole application of each treatment on Calu-6 cell line, an epithelial cell line of human lung carcinoma, and the expression of Cdc42 gene. The viability of Calu-6 was examined after 24- or 48-hour treatment with doses of 0.5 to 8 µg/ml of curcumin, 0.1 to 50 µg/ml of cisplatin and combined doses of curcumin and Cisplatin by MTT assay. To measure apoptosis and the expression of Cdc42 gene, flow cytometry and Real-Time PCR were utilized. Decrease of cell viability and induction of cell death were observed in the cells treated with 0.67 µg/ml of curcumin and 1.7 µg/ml of cisplatin (the lowest effective dose) and the combined treatment with the same doses of each drug after 24-hour treatments. The maximum rates of early and late apoptosis were related to treatment with curcumin and the combined treatment. The gene expression analysis results indicated that both Curcumin and Cisplatin decrease the expression of Cdc42 gene, moreover, their co-administration showed synergic effects. Therefore, Curcumin could be an appropriate option for complementary administration with other chemotherapy agents in order to reduce their efficient dose, and to reduce their side effects.
 
 

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Pancreatic cancer is one of the most deadly and aggressive cancers; Fluorouracil induces apoptosis and cell cycle arrest in cancer cells. In the present study; the effect of Fluorouracil on different stages of the cell cycle and the expression of genes involved in the internal pathway of apoptosis in the AsPC-1 cell line (human pancreatic cancer) were investigated. In order to do so, MTT assay was used to evaluate the cytotoxic effect of Fluorouracil on AsPC-1 cell proliferation; The type of induced cell death and cell cycle changes were investigated by flow cytometry; changes in the expression level of genes (BAX, Bcl-2, APAF-1, Caspase-3, Caspase-9, p53, p21) were examined by Real-time PCR. Quantitative data were analyzed at the significant level of (p<0.05). The MTT assay results showed that Fluorouracil decreased AsPC-1 cell proliferation in a concentration-dependent manner. The results of flow cytometry analysis showed that increased percentage of apoptotic cells in the treated cells; Fluorouracil induces S phase cell cycle arrest in AsPC-1 cells and reduced distribution in the G1 phase. The Real-time PCR results in treated cells showed an increase in the expression of genes in the mitochondrial apoptotic pathway as well as genes effective in regulating the cell cycle. Fluorouracil reduces cell proliferation and induces apoptosis by increasing the expression of genes involved in the Intrinsic apoptotic pathway in AsPC-1 cells; Fluorouracil also caused cell cycle arrest in these cells by regulating the (p53, p21) genes.