Effect of diallyl disulfide on insulin-like growth factor signaling molecules involved in cell survival and proliferation of human prostate cancer cells in vitro and in silico approach through docking analysis

Ramachandran, A.; Sharmila, Govindaraj; Elumalai, Perumal; Kalimuthu, S; Banudevi, Sivanantham; Gunadharini, Dharmalingam Nandagopal; Benson, Chellakan Selvanesan; Daisy, P.; Arunakaran, J.

doi:10.1016/j.phymed.2012.04.009

Cited by 43 publications

(20 citation statements)

References 41 publications

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“…Apoptosis induction involves different apoptotic genes and enzymes depending on the cell type of different tumors (16). DADS has the ability to induce apoptosis of human tumor cells including those of colon, gastric, prostate and breast origin (10,11,18,(20)(21)(22). Our study confirmed the apoptotic effects of DADS on ECA109 cells by using several methods.…”

Section: Discussionsupporting

confidence: 74%

“…DADS has a wide variety of biological activities including antifungal (5), antibacterial (6), antiviral (7), antioxidant (8), antiplatelet and antithrombotic properties (9). Moreover, DADS has gained increasing attention due to its protective effects of cancer development and anticancer effects against different types of malignancies (10)(11)(12)(13). Notably, the apoptotic effects of DADS were even superior to those of chemotherapy agents such as 5-Fu and CTX in human breast cancer cells (14).…”

Section: Introductionmentioning

confidence: 99%

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Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma

et al. 2014

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Abstract. Esophageal squamous cell carcinoma (ESCC) is an aggressive tumor with high incidence and mortality worldwide. Diallyl disulfide (DADS) is a natural organosulfur compound, isolated from garlic. In this study, MTT assay showed that DADS significantly reduced cell viability in a dose-and timedependent manner in ESCC cells, with lower toxicity in normal liver cells. Cell cycle analysis revealed that DADS made G2/M phase arrest. Molecular analysis suggested that this cell cycle arrest was likely made by the decrease of cyclin B1, cdc2, p-cdc2, cdc25c in concomitance with activation of the p53/p21 pathway. Apoptosis was detected by Annexin V/PI staining. The molecule markers showed that DADS induced apoptosis through activating caspases, altering the Bax/Bcl-2 balance and suppressing the MEK-ERK pathway. Our data indicated that DADS has the potential to be an effective and safe anticancer agent for ESCC therapy in the near future.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma

et al. 2014

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“…Previous studies showed that DADS suppressed the proliferation of cancer cell through cell cycle arrest and apoptosis. 13,31,32 Classical theories hypothesize that cell cycle arrest is a mechanism of self-protection, to enable sufficient time to repair DNA damage. If cells are efficiently repaired, they will reenter the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

Diallyl disulfide enhances carbon ion beams–induced apoptotic cell death in cervical cancer cells through regulating Tap73 /ΔNp73

Chen

Sun

et al. 2015

Cell Cycle

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Diallyl disulfide (DADS), extracted from crushed garlic by steam-distillation, has been reported to provide the anticancer activity in several cancer types. However, the effect of DADS on high-LET carbon beams -induced cell death remains unknown. Therefore, we used human cervical cancer cells to elucidate the molecular effects of this dallyl sulfide. Radiotherapy remains the mainstay of treatment, especially in advanced cervical cancer and there is still space to improve the radiosensitivity to reduce radiation dosage. In this study, we found that radiation effects evoked by high-LET carbon beam was marked by inhibition of cell viability, cell cycle arrest, significant rise of apoptotic cells, regulation of transcription factor, such as p73, as well as alterations of crucial mediator of the apoptosis pathway. We further demonstrated that pretreatment of 10 mM DADS in HeLa cells exposed to radiation resulted in decrease in cell viability and increased radiosensitivity. Additionally, cells pretreated with DADS obviously inhibited the radiationinduced G2/M phase arrest, but promoted radiation-induced apoptosis. Moreover, combination DADS and the radiation exacerbated the activation of apoptosis pathways through up-regulated ration of pro-apoptotic Tap73 to antiapoptotic DNp73, and its downstream proteins, such as FASLG, and APAF1. Taken together, these results suggest that DADS is a potential candidate as radio sensitive agent for cervical cancer.

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“…For the past 30 years, studies have explored the use of diallyl disulfide (DADS), the main active component of the cancer-fighting allyl sulfides found in garlic, as it has been shown to reduce the initiation of carcinogen-induced cancers and inhibit the proliferation of various types of cancer cells (4). The actions of DADS include the regulation of cell cycle arrest, induction of apoptosis and cell differentiation, and inhibition of cell invasion (5–7).…”

Section: Introductionmentioning

confidence: 99%

Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells

et al. 2016

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Abstract. Diallyl disulfide (DADS) has shown potential as a therapeutic agent in various cancers. Previously, calreticulin (CRT) was found to be downregulated in differentiated HL-60 cells treated with DADS. The present study investigated the role of CRT proteins in DADS-induced proliferation, invasion and differentiation in HL-60 cells. The present study demonstrated that DADS treatment significantly changed the morphology of HL-60 cells and caused the significant time-dependent downregulation of CRT. Small interfering RNA (siRNA)-mediated knockdown of CRT expression significantly inhibited proliferation, decreased invasion ability, increased the expression of cluster of differentiation (CD)11b and reduced the expression of CD33 in DADS-treated HL-60 cells. DADS also significantly affected cell proliferation, invasion and differentiation in CRT-overexpressed HL-60 cells. Nitroblue tetrazolium (NBT) reduction assays showed decreased NBT reduction activity in the CRT overexpression group and increased NBT reduction in the CRT siRNA group. Following treatment with DADS, the NBT reduction abilities in all groups were increased. In conclusion, the present study clearly demonstrates the downregulation of CRT during DADS-induced differentiation in HL-60 cells and indicates that CRT is involved in cell proliferation, invasion and differentiation in DADS-treated HL-60 cells. IntroductionAcute myeloid leukemia (AML) is a genetically heterogeneous clonal disorder caused by the build up of somatic mutations in hematopoietic progenitor cells, which affects the regulation of self-renewal, survival, proliferation and differentiation (1).The induction of differentiation is a desired consequence of chemopreventive and therapeutic agents, as it often results in the elimination of premalignant or malignant cells (2). Numerous studies focus on selectively killing tumor cells through differentiation induction (3). Therefore, the development of novel differentiation-inducing drugs for blocking AML is of clinical significance.For the past 30 years, studies have explored the use of diallyl disulfide (DADS), the main active component of the cancer-fighting allyl sulfides found in garlic, as it has been shown to reduce the initiation of carcinogen-induced cancers and inhibit the proliferation of various types of cancer cells (4). The actions of DADS include the regulation of cell cycle arrest, induction of apoptosis and cell differentiation, and inhibition of cell invasion (5-7). Previous studies at the Cancer Research Institute, University of South China (Hengyang, China) confirmed that DADS can inhibit the proliferation of human leukemia cells in vivo in a dose-dependent manner (8,9). DADS exhibits a dual effect: A medium dose (>1.25 mg/l) can induce apoptosis in human leukemia cells (8,9), and a small dose (<1.25 mg/l) can induce human leukemia cell differentiation (2). The mechanisms of inducing differentiation involve: G 2 /M-phase cell cycle arrest; histone acetylation; the regulation of regulatory gene expression, including signa...

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Effect of diallyl disulfide on insulin-like growth factor signaling molecules involved in cell survival and proliferation of human prostate cancer cells in vitro and in silico approach through docking analysis

Cited by 43 publications

References 41 publications

Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma

Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma

Diallyl disulfide enhances carbon ion beams–induced apoptotic cell death in cervical cancer cells through regulating Tap73 /ΔNp73

Involvement of calreticulin in cell proliferation, invasion and differentiation in diallyl disulfide-treated HL-60 cells

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