Background: Herbal compounds are attractive anticancer candidates due to their low toxicity. Pervious studies have demonstrated that Hibiscus sabdariffa is promising as an anticancer agent against several cancer types; however, its potential therapeutic role in breast cancer remains to be investigated. Materials and Methods: In the present study, the cytotoxic effects of Hibiscus sabdariffa aqueous extract (HSE) on a human breast adenocarcinoma cell line (MCF-7) and fetal foreskin fibroblast (HFFF) were investigated. Different concentrations of water extract of calyces were added and the percentage of cell survival was determined after 24, 48, and 72 hours using an MTT assay. Apoptosis induction was assessed by DNA fragmentation. Results: At the concentration of 0.5 mg/ml of the extract and following 72 hours of incubation, the number of viable MCF-7 cells was less than 50%. The extract was not cytotoxic against normal HFFF cells in all tested concentrations. Also, HSE induced apoptosis only in MCF-7 cells. Conclusions: These results suggest that HSE inhibits the growth of MCF-7 cells selectively in a concentration- and time-dependent manner. As this herbal substance has been shown to be nontoxic at very high doses in experimental animals, it might be a good anticancer drug candidate for breast cancer treatment
Background: Osteosarcoma (OS) is the most common type of bone malignancy. Many studies have attempted to find the association between microRNAs and cancer-associated processes. Alterations in miRNA expression through genetic or epigenetic changes, impairment of transcription factors, and ectopic expression of miRNAs induce the development and progression of cancer. Although miR-135b has been thoroughly documented as an oncogene in the majority of studies, some controversies remain about the conflicting role of miR-135b as a tumor-suppressor. Objectives: The present study aimed at investigating the oncogenic and/or tumor-suppressing role of miR-135b in human OS. Methods: In this study, 21 OS tissue samples, along with 21 adjacent bone tissues (normal) as control specimens were collected to analyze the expression of miR-135b. The Saos2 cell-line was transiently transfected with the miR-135b mimic and inhibitor to assess its effect on two critical transcription factors, namely FOXO-1 and c-Myc. qRT-PCR was performed to quantify the expression of miR-135b in both OS tissues and the Saos2 cell-line. The MTT, cell migration, and cell invasion assays were used to characterize the miR-135b function. The western blot analysis was carried out to monitor the targets of miR-135b. Finally, the changes in cellular functions such as migration and invasion, following the transfection of miR-135b mimic and inhibitor, were verified. Results: The results showed that in comparison with the adjacent normal bone tissues, the expression of miR-135b was higher in OS tissue samples, which inversely correlated with the expression rate of FOXO-1, whereas the expression of c-Myc had a direct relationship to miR-135b expression. Functionally, the miR-135b mimic led to an increase in cell proliferation, invasion, and migration of OS cancer cells. Conclusions: MiR-135b induces the proliferation and invasion of OS cells by the degradation of FOXO-1 and upregulation of c-Myc.
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