Background:Breast cancer is the second leading cause of cancer-related death among females in the world. To date, chemotherapy has been the most frequently used treatment for breast cancer and other cancers. However, some natural products have been used, as alternative treatments for cancers including breast cancer, due to their wide range of biological activities and low toxicity in animal models.Objectives:The present study examined the anti-proliferative activity of curcumin and its effect(s) on the apoptosis of breast cancer cells.Materials and Methods:This study was performed by an in vitro assay and the anticancer effects of curcumin were determined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide). We used quantitative real time Polymerase Chain Reaction (PCR) for detection of Mcl-1 gene expression in treated groups and then compared them to control samples.Results:In the treatment group, there were higher levels of cell death changes than the control group. The results also showed that the Mcl-1 gene expression declined in the tested group as compared to the control group.Conclusions:Our present findings indicated that curcumin significantly inhibited the growth of human breast cancer cell MCF-7 by inducing apoptosis in a dose- and time- dependent manner, accompanied by a decrease in MCF-7 cell viability. Furthermore, our results showed that quantitative real-time PCR could be used as a direct method for detection Mcl-1 gene expression in tested samples and normal samples.
Autophagy is an evolutionarily conserved process that plays a role in regulating homeostasis under physiological conditions. However, dysregulation of autophagy is observed in the development of human diseases, especially cancer. Autophagy has reciprocal functions in cancer and may be responsible for either survival or death. Hepatocellular carcinoma (HCC) is one of the most lethal and common malignancies of the liver, and smoking, infection, and alcohol consumption can lead to its development. Genetic mutations and alterations in molecular processes can exacerbate the progression of HCC. The function of autophagy in HCC is controversial and may be both tumor suppressive and tumor promoting. Activation of autophagy may affect apoptosis in HCC and is a regulator of proliferation and glucose metabolism. Induction of autophagy may promote tumor metastasis via induction of EMT. In addition, autophagy is a regulator of stem cell formation in HCC, and pro-survival autophagy leads to cancer cell resistance to chemotherapy and radiotherapy. Targeting autophagy impairs growth and metastasis in HCC and improves tumor cell response to therapy. Of note, a large number of signaling pathways such as STAT3, Wnt, miRNAs, lncRNAs, and circRNAs regulate autophagy in HCC. Moreover, regulation of autophagy (induction or inhibition) by antitumor agents could be suggested for effective treatment of HCC. In this paper, we comprehensively review the role and mechanisms of autophagy in HCC and discuss the potential benefit of targeting this process in the treatment of the cancer.
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Background: Prostate Cancer (PCa) is the major reason for the high mortality rates among men worldwide. In fact, current therapeutic approaches are not successful. It appears that discovering more effective methods considering several parameters such as availability, low cost, and no toxicity to normal cells is one of the biggest challenges for interested researchers. Green tea (extracted from the plant Camellia sinensis) with high level of polyphenolic compounds and as the most globally consumed beverage has attracted considerable interest. MicroRNAs (or miRNAs) were considered as novel tools in cancer therapy which modulate various biological events in cell by regulation of gene expression. The aim of the current study was to evaluate the antitumor activity of green tea in LNCaP cells through up-regulation of miR-181a expression.
Methods: First, LNCaP cells were cultured and by using quantitative real time PCR (qRT-PCR) and western blot methods, the expression levels of Bax and BCL2 were analyzed. Next, a 3D cell culture model was applied to evaluate the expression of miRNA-181a in LNCaP cells.
Results: It was shown that green tea induced cellular apoptosis. The high number of apoptotic nuclei was also shown by using DAPI staining. The inhibition of tumor growth was revealed by analyzing the size and number of spheroids. Also, up-regulation of miR-181a expression in LNCaP cells was revealed after treatment with green tea.
Conclusion: Our results are helpful to design antitumor regimens based on consumption of green tea through up-regulation of miRNA-181a expression and induction of apoptosis.
Background: Anti-proliferative effects of probiotics are considerable in the treatment of various cancers, including colon cancer. In the present study, two new Lactobacillus strains as probiotics were isolated from stool samples at a clinical lab. Objectives: The aim of this study was to evaluate the effects of the cell-free lyophilized filtrate of two new strains of Lactobacillus, isolated on viability on Caco-2 cells. Methods: Two new strains of Lactobacillus were isolated from 1 gr of each infant stool specimens from a total of fifty volunteers, according to the principles of a scientific questionnaire. The anti-proliferative effects of the strains were investigated using the MTT assay with Caco-2 cell lines. Results: Out of 50 samples, seven isolates were lactic acid bacteria, two strains of which were probiotics related to L. fermentum (E) and L. rhamnosus (G). The results showed that the two Lactobacillus strains had good anti-proliferative effects against the cancer cell lines tested. These strains were resistant to low pH and 0.3% bile salt. Cytotoxicity assay revealed that the most effective concentration of strains E (~55% to~72%) and G (~60% to~80%) on Caco-2 cells was 10000 µg/mL after 24 to72 hours. Conclusions: Cytotoxicity effect of the cell-free lyophilized filtrate of bacteria on Caco-2 cells in a dose-and time-dependent manner suggested that these strains might be used in colon cancer therapy.
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