Low-dose all-trans retinoic acid enhances cytotoxicity of cisplatin and 5-fluorouracil on CD44+ cancer stem cells

Najafzadeh, Nowruz; Mazani, Mohammad; Abbasi, Asadollah; Farassati, Faris; Amani, Mojtaba

doi:10.1016/j.biopha.2015.08.019

Cited by 34 publications

(19 citation statements)

References 37 publications

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“…As reported, some studies showed that adapalene induced apoptosis and G1 phase arrest in the colorectal carcinoma cells . Dramatically, the studies in regard to other retinoids all showed G1 or G2 phase arrest in several kinds of tumor cells, including skin cancers . However, the effect of remarkable S‐phase arrest was detected in our results by flow cytometry using PI staining.…”

Section: Discussioncontrasting

confidence: 43%

The third‐generation retinoid adapalene triggered DNA damage to induce S‐phase arrest in HaCat cells

Wang

et al. 2019

Fundamemntal Clinical Pharma

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Epidermal proliferative diseases consisted of a series of common skin diseases, most of which were recurrent chronic skin diseases, and had greatly negative influence on the life quality of patient. Retinoids exhibited vital roles in the treatment of many skin diseases. Our recent study demonstrated that adapalene significantly inhibited the growth of HaCat cells, and the inhibitory activity was stronger than other retinoids, such as all-trans-retinoic acid, acitretin, isotretinoin, tazarotene, and bexarotene. Further study showed that adapalene suppressed the colony formation of HaCat cells, and it dramatically triggered S-phase arrest and apoptosis, rather than G1 phase arrest which was reported in other retinoids in several studies. Additionally, adapalene treatment greatly upregulated the protein expression of DNA damage marker c-H2AX, which was in accord with the results of the elongation of tail moment by comet electrophoresis analysis. Moreover, DNA damage was triggered and DNA repair was suppressed synchronously with adapalene treatment, which accounted for the mechanism of S-phase arrest induced by adapalene. In summary, our recent work demonstrated that adapalene showed strong antiproliferation activity in HaCat cells and could be an alternative agent for the epidermal proliferative disease. I N T R O D U C T I O NEpidermal proliferative diseases were a large class of dermatosis which contained various common and uncommon skin diseases such as psoriasis, verruca vulgaris, pityriasis rubra pilaris, and palmoplantar keratoderma. Moreover, most of the epidermal proliferative diseases were recurrent chronic skin diseases which seriously affected the life quality of patients. Long-term clinical practice showed that oral or topical retinoids were a kind of effective and relatively safe therapy for these diseases. Retinoids were a serious of natural or synthetic derivatives of retinol which played vital roles in the differentiation and proliferation of epidermal cells, and made great influence on the formation, development and maintenance of normal epidermis. In addition, retinoids were also widely used for the experiments of diverse human cancers due to their influences on the cell proliferation and apoptosis of multiple tumor cells [1]. Currently, the commonly used retinoids were alltrans-retinoic acid (ATRA), acitretin, isotretinoin, and tazarotene [2][3][4][5][6][7][8]. However, repeated and long-term use of these drugs often caused a lot of adverse reactions like allergic reaction, dry skin, piercing, photosensitivity, and skin infection. More importantly, the teratogenicity of retinoids could not be ignored. Hence, the high-efficiency and low-adverse-reaction drugs remained the pursuit of the clinical application.Adapalene, the third-generation synthetic retinoic acid, was hardly absorbed into blood circulation and ª 2019 Soci et e Franc ßaise de Pharmacologie et de Th erapeutique 380

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Section: Discussioncontrasting

confidence: 43%

The third‐generation retinoid adapalene triggered DNA damage to induce S‐phase arrest in HaCat cells

Wang

et al. 2019

Fundamemntal Clinical Pharma

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“…Recent studies have shown that phytochemicals can restore the sensitivity of cancer cells to conventional chemotherapeutic drugs [ 18 ]. Synergistic or additional effects of combinations of DDP and phytochemical compounds in cancer cells with acceptable side effects have also been demonstrated [ 19 , 20 ]. Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide, CAP) is one of the major pungent ingredients of red pepper and has been widely used in clinical medicine for the treatment of pain and inflammation caused by various diseases [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Synergistic inhibitory effects of capsaicin combined with cisplatin on human osteosarcoma in culture and in xenografts

Wang

Deng

Chang

et al. 2018

J Exp Clin Cancer Res

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BackgroundThe combination of phytochemicals with chemotherapy drugs is an emerging new strategy for cancer therapy to increase antitumor responses.MethodsThe present study investigates the effect of the combination of capsaicin (CAP) with cisplatin (DDP) and the potential underlying anticancer mechanisms in osteosarcoma (OS) cells in vitro and in vivo.ResultsCell viability assays and isobolographic analyses demonstrated that the combination of CAP and DDP showed synergistic cytotoxic effects on OS cells. We chose relatively low concentrations of CAP (100 μM) and DDP (16.7 μM) for subsequent experiments. Generally, the combination of CAP and DDP had significant effects on apoptosis induction, cell cycle arrest and cell invasion inhibition in OS cells compared with the individual-treatment groups and the control group. Moreover, cotreatment with CAP and DDP triggered prosurvival autophagy through reactive oxygen species (ROS)/JNK and p-AKT/mTOR signaling in OS cells. The combination regimen of CAP and DDP also inhibited tumor growth in an OS xenograft model.ConclusionThese results suggest that the combination of CAP and DDP has strong inhibitory effects on OS cells and identify CAP as a promising agent for supplementing standard chemotherapy and possible future targeted therapy in OS.

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“…In a study, Najafzadeh et al planned a survey to determine the combination of ATRA as potent anticancer and chemotherapeutic drugs such as cisplatin and 5-fluorouracil to increase the efficacy of the drugs. They pretreated the cancer cells at low dose ATRA for 7 days [16], but in the present study, we pretreated the melanoma cells for a short time (4 h). Our results elucidated that a high dose of ATRA (for 4 h) highly promotes the apoptotic effects of dacarbazine, which may be due to apoptosis and cell cycle arrest.…”

Section: Discussionmentioning

confidence: 99%

“…This limitation may be overcome by using a combination of lower dosages of chemotherapy agents. Studies have shown that ATRA combination with chemotherapy agents can inhibit the proliferation of gastrointestinal cancers [16], ovarian adenocarcinoma, and squamous head and neck cancers [17].…”

Section: Introductionmentioning

confidence: 99%

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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Low-dose all-trans retinoic acid enhances cytotoxicity of cisplatin and 5-fluorouracil on CD44+ cancer stem cells

Cited by 34 publications

References 37 publications

The third‐generation retinoid adapalene triggered DNA damage to induce S‐phase arrest in HaCat cells

The third‐generation retinoid adapalene triggered DNA damage to induce S‐phase arrest in HaCat cells

Synergistic inhibitory effects of capsaicin combined with cisplatin on human osteosarcoma in culture and in xenografts

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

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