Molecular mechanism and cytotoxicity of allicin and all-trans retinoic acid against CD44+ versus CD117+ melanoma cells

Jobani, Bahareh Mohammadi; Najafzadeh, Nowruz; Mazani, Mohammad; Arzanlou, Mohsen; Mohammadzadeh-Vardin, Mohammad

doi:10.1016/j.phymed.2018.05.013

Cited by 27 publications

(25 citation statements)

References 33 publications

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“…It has been reported that ATRA combinations with other drugs has cytotoxic effects on several cancer cell lines [22,23]. In the previous study, we showed that ATRA was more effective to inhibit proliferation of CD117 + cells than CD44 + cells in the A375 melanoma cell line [18]. This study extended prior work by revealing the response of CD117 + cells to short-term ATRA pretreatment and dacarbazine.…”

Section: Discussionsupporting

confidence: 79%

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In Vitro Anticancer Effects of All-trans Retinoic Acid in Combination with Dacarbazine against CD117+ Melanoma Cells

2020

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Background Malignant melanoma is a common form of skin cancer that contains different cell types recognized by various cell surface markers. Dacarbazine-based combination chemotherapy is frequently used for the treatment of melanoma. Despite its potent anticancer properties, resistance to dacarbazine develops in malignant melanoma. Here, we aim to improve response to dacarbazine therapy by pretreatment with all-trans retinoic acid (ATRA) in CD117+ melanoma cells. Methods The CD117+ melanoma cells were sorted from A375 malignant melanoma cell line using magnetic-activated cell sorting (MACS). The cell viability was examined by cell proliferation assay (MTT). Apoptosis was determined by acridine orange/ ethidium bromide staining. Indeed, we performed flow cytometry to evaluate the cell cycle arrest. Results Here, the CD117+ melanoma cells were incubated with various concentrations of ATRA, dacarbazine, and their combination to determine IC50 values. We found that 20 µM ATRA treatment followed by dacarbazine was found to be more effective than dacarbazine alone. There was an indication that the combination of ATRA with dacarbazine (ATRA/dacarbazine) caused more apoptosis and necrosis in the melanoma cells (P<0.05). Furthermore, ATRA/dacarbazine treatment inhibited the cell at the G0/G1 phase, while dacarbazine alone inhibited the cells at S phase. Conclusion Collectively, combined treatment with ATRA and dacarbazine induced more apoptosis and enhanced the cell cycle arrest of CD117+ melanoma cells. These results suggested that ATRA increased the sensitivity of melanoma cells to the effect of dacarbazine.

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Section: Discussionsupporting

confidence: 79%

“…The CD117 + cells were isolated from the A375 melanoma cell line as previously described [18,20]. The melanoma cells were harvested, prepared into single-cell suspension, and counted.…”

Section: Separation Of Cd117 + Cells By Macsmentioning

confidence: 99%

In Vitro Anticancer Effects of All-trans Retinoic Acid in Combination with Dacarbazine against CD117+ Melanoma Cells

2020

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“…Schultz et al demonstrated the activity of allicin in inhibiting ornithine decarboxylase, a rate-limiting enzyme in cell proliferation of neuroblastoma, and inducing cell apoptosis [111]. Moreover, allicin suppresses melanoma cell growth via increasing cyclin D1 and reducing MMP-9 mRNA expression [112]. It also inhibits human glioblastoma proliferation by stimulating S and G 2 /M phase cell cycle arrest, apoptosis, and autophagy [113].…”

Section: Allicinmentioning

confidence: 99%

Plant-Derived Natural Products in Cancer Research: Extraction, Mechanism of Action, and Drug Formulation

et al. 2020

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Cancer is one of the main causes of death globally and considered as a major challenge for the public health system. The high toxicity and the lack of selectivity of conventional anticancer therapies make the search for alternative treatments a priority. In this review, we describe the main plant-derived natural products used as anticancer agents. Natural sources, extraction methods, anticancer mechanisms, clinical studies, and pharmaceutical formulation are discussed in this review. Studies covered by this review should provide a solid foundation for researchers and physicians to enhance basic and clinical research on developing alternative anticancer therapies.

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“…Fold changes were calculated using the comparative Ct method. The relative amount of the targeted gene's transcripts was normalized by the amount of GAPDH transcript in the same cDNA [15].…”

Section: Quantification Of Gene Expression By Real-time Pcrmentioning

confidence: 99%

Efficacy of Metformin and Chemotherapeutic Agents on the Inhibition of Colony Formation and Shh/Gli1 Pathway: Metformin/Docetaxel Versus Metformin/5-Fluorouracil

et al. 2020

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Background Gastric cancer is a common gastrointestinal cancer characterized by poor prognosis and chemoresistance. Docetaxel and 5-fluorouracil (5-FU) are frequently used for the treatment of gastric cancer. Despite their potent anti-cancer effects, chemoresistance occurs in metastatic gastric cancer. Metformin, a popular anti-diabetic drug, has been proven to have potent anticancer effects on gastrointestinal cancers. Here, we aim to improve this chemotherapy agents’ efficacy by pretreatment with metformin. Methods The AGS gastric cancer cell line were pretreated with three different sub-toxic concentration of metformin and then treated with various concentrations of 5-FU and docetaxel.The anticancer effects of the combination of metformin with the chemotherapy agents were determined using clonogenic assay and DAPi staining. We used real-time PCR to evaluate Gli1, Gli2, and TWIST1 mRNA expression levels in the gastric cancer cells. Also, the expression of the Shh protein was assessed using immunocytochemistry. Results Here, we found that metformin sensitized the gastric cancer cells to chemotherapy. The combination treatments were more effective in reducing the number of cancer colonies compared to 5-FU or docetaxel alone. The combination of metformin with 5-FU or docetaxel significantly reduced the number of cells expressing the Shh protein compared to the 5-FU alone or docetaxel alone. Interestingly, we found that the combination of metformin with docetaxel significantly down-regulated the mRNA levels of Gli1, Gli2, and TWIST1 in the AGS gastric cancer cell line compared to docetaxel alone. Conclusion Overall, our data strongly support an important role for metformin as an enhancer of the efficacy of chemotherapeutic agents against gastric cancer.

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Molecular mechanism and cytotoxicity of allicin and all-trans retinoic acid against CD44+ versus CD117+ melanoma cells

Cited by 27 publications

References 33 publications

In Vitro Anticancer Effects of All-trans Retinoic Acid in Combination with Dacarbazine against CD117+ Melanoma Cells

In Vitro Anticancer Effects of All-trans Retinoic Acid in Combination with Dacarbazine against CD117+ Melanoma Cells

Plant-Derived Natural Products in Cancer Research: Extraction, Mechanism of Action, and Drug Formulation

Efficacy of Metformin and Chemotherapeutic Agents on the Inhibition of Colony Formation and Shh/Gli1 Pathway: Metformin/Docetaxel Versus Metformin/5-Fluorouracil

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