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This study investigated the potential of Persian shallot extract as an anticancer agent in HepG2 tumor cell line, an in vitro human hepatoma cancer model system. The inhibitory effect of Persian shallot on the growth of HepG2 cells was measured by MTT assay. To explore the underlying mechanism of cell growth inhibition of Persian shallot, the activity of Persian shallot in inducing apoptosis was investigated through the detection of annexin V signal by flow cytometry and expression of some apoptosis related genes such p21, p53, puma, caspase-8 family-Bcl-2 proteins like bid, bim, bcl-2 and bax were measured by real-time PCR in HepG2 cells. Persian shallot extract inhibited the growth of HepG2 cells in a dose-dependent manner. The IC value (inhibiting cell growth by 50%) was 149 μg/ml. The results of real-time PCR revealed a significant up-regulation of bid, bim, caspase-8, puma, p53, p21 and bax genes and a significant downregulation of bcl-2 gene in HepG2 cells treated with Persian shallot extract significantly. Therefore, this is the first report on an increased expression of bid, bim, caspase-8, puma, p53, p21 and bax genes and down regulation of bcl-2 gene indicating that the Persian shallot extract possibly induced the process of cell death through the intrinsic and extrinsic apoptosis pathways and triggers the programmed cell death in HepG2 tumor cell lines by modulating the expression of pro-/anti-apoptotic genes. Furthermore, we showed that Persian shallot extract increased annexin V signal and expression, resulting in apoptotic cell death of HepG2 cells after 24 h treatment. Therefore, according to the results of this study, the Persian shallot extract could be considered as a potential candidate for production of drug for the prevention or treatment of human hepatoma.

Hepatocellular carcinoma (HCC) is a prevalent human malignancy which its drug resistance is increasing world-wide. This project was designed to assess the anti-cancer effects of 4-bromo-2-(((5-chloro-2-hydroxyphenyl) imino) methyl) phenol ([IV(L)] complex) on the HepG2 cell line and also L929 cells, as normal cells. HepG2 and L929 cells were cultured in RPMI culture medium and the survival rates of the cells were determined after 24 and 48 h using MTT assay to find IC50 concentration of vanadium m, [IV(L)] complex. The early apoptosis and necrosis/late apoptosis were determined by means of annexin V/PI apoptosis detection kit. The results revealed that vanadium m, [IV(L)] complex induce early apoptosis higher in HepG2 cell line than L929 cells. The rates of necrosis/late apoptosis were also induced in HepG2 cells more than L929 cells. Based on the results, vanadium m, [IV(L)] complex might be considered as a safe new drug for treatment of HCC with low side effects on control liver cells.

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Background: Breast cancer is one of the most malignant cancers in the world. Cold micro plasma jet (CMPJ) Known as cold atmospheric jet microplasma, it has recently been introduced as an alternative way to overcome the challenges of finding an effective cancer treatment. Numerous studies have reported promising results, so our aim of this study was to investigate how this method affects cell death and its role on the expression of apoptotic genes in the MCF-7 cancer cell line. Methods: In this study, helium gas was used to generate plasma at room temperature in the form of point radiation at different times of 30, 60, 90 and 120 seconds and at different distances of 1 cm. Flow cytometry will be used to examine the extent of apoptosis and necrosis. Genes involved in apoptosis P53, P21, Bax and Bcl-2 were measured by real-time PCR. Results: Our Studie indicate that the mechanism of action of cold plasma on cancer cells is related to generation of reactive oxygen species with possible induction of the apoptosis pathway. The percentages of necrotic and late apoptotic cells following treatment with different times plasma (0, 30, 60, 90 and 120 s) were about 0.55 ± 0.06, 20.13 ± 0.01, 20.12 ± 0.03, 26.81 ± 0.04 and 17.51 ± 0.05. The mRNA expression of bcl-2 showed a decrease of 90s of plasma while the mRNA expression of p53, bax and caspase-8 genes increased compared to untreated cells. Conclusion: In general, research in the last decade has confirmed the ability of CMPJ as an effective anti-cancer tool. Therefore, it may be used to help treat cancer. However, its clinical application requires much further studies to determine the severity and duration of exposure to CMPJ for effective treatment based on the type of cancer.