Combinative effects of β-Lapachone and APO866 on pancreatic cancer cell death through reactive oxygen species production and PARP-1 activation

Breton, Caroline; Aubry, Dominique; Ginet, Vanessa; Puyal, Julien; Heulot, Mathieu; Widmann, Christian; Duchosal, Michel A.; Nahimana, Aimable

doi:10.1016/j.biochi.2015.07.012

Cited by 16 publications

(16 citation statements)

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“…A particularly intriguing aspect of tumorigenesis is the accumulative capacity of the cellular genome to further respond to DNA damage and also the characterization of particular suppressor genes or oncogenes to substantially support mutability of essentially susceptibility of DNA to further malignant transformation. Combined effects of beta-Lapachone and APO866 on pancreatic cancer cell death via reactive oxygen species production and activated PARP1 [15] may prove significant.…”

Section: Promotional Susceptibilitiesmentioning

confidence: 99%

Strictly Approximating Attributes of DNA Lesion Repair in Terms of Inherent DNA Responses to Mutability and Malignant Transformation

2017

MJCCS

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Selective susceptibilities of the cellular genome for permissive emergence of mutability hot-spots are governed by specific patterns of approximate repair of lesions in terms of response to DNA damage. Given the pattern recognition of mutability as an integral approximation there is central cooperative susceptibility within such pattern responses that specify the attributes of genomic instability as contexts for approximate DNA repair. Malignant transformation is hence a para-physiologic consequence for permissive evolution of the malignant transformation of cells and for the creation of a milieu for permissive accumulation of mutability susceptibilities towards malignancy.

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Section: Promotional Susceptibilitiesmentioning

confidence: 99%

Strictly Approximating Attributes of DNA Lesion Repair in Terms of Inherent DNA Responses to Mutability and Malignant Transformation

2017

MJCCS

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“…[14] Pharmacological drugs are in various stages of clinical research, involved in depletion or inhibition of antioxidant systems. Exogenous ROS-inducing agents like gadolinium texaphyrin [17] and -Lapachone (ARQ 501) [18] have also shown similar anticancer efficacy. Exogenous ROS-inducing agents like gadolinium texaphyrin [17] and -Lapachone (ARQ 501) [18] have also shown similar anticancer efficacy.…”

Section: Introductionmentioning

confidence: 99%

“…In the present study, we show prooxidant ability of ascorbic acid, which enhances cytotoxicity induced by juglone. Exogenous ROS-inducing agents like gadolinium texaphyrin [17] and -Lapachone (ARQ 501) [18] have also shown similar anticancer efficacy. This combination also affects enzyme activity of catalase, glutathione reductase, and superoxide dismutase destabilizing redox balance in cell and thereby making juglone effective at a lower dose.…”

mentioning

confidence: 99%

Juglone–ascorbic acid synergy inhibits metastasis and induces apoptotic cell death in poorly differentiated thyroid carcinoma by perturbing SOD and catalase activities

Gaikwad

Salwe

et al. 2018

J Biochem & Molecular Tox

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Anaplastic thyroid carcinoma (ATC) requires more innovative approaches as the current regimes for therapy are inadequate, also most anticancer drugs cause general suppression of physiological functions. However, therapy with limited nontarget tissue damage is desirable. In the present study, we show prooxidant ability of ascorbic acid, which enhances cytotoxicity induced by juglone. We decipher that juglone-ascorbate combination induces reactive oxygen species-mediated apoptosis leading to cell death in ARO cell line originated from ATC. This combination also affects enzyme activity of catalase, glutathione reductase, and superoxide dismutase destabilizing redox balance in cell and thereby making juglone effective at a lower dose. We also show that juglone-ascorbate combination suppresses cell migration, invasion, and expression of tumor-promoting, and angiogenic genes in ARO cell line, thereby disrupting epithelial-mesenchymal transition ability of the cells. Overall, we show that ascorbic acid increases cytotoxic potency of juglone through redox cycling when used in synergy.

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“…In the last decade, many studies to elucidate the effect of bL on cancer development have been conducted and have shown that bL has an inhibitory effect on various cancers such as epidermoid laryngeal cancer [15] and prostate [16][17][18][19], colon [20,21], ovarian [19], lung [22], and breast cancer [23]. bL has been identified to suppress cancer proliferation by directly interacting with and inhibiting the catalytic activity of DNA topoisomerase I [24], by inducing apoptosis or necrosis by releasing mitochondrial cytochrome C from mitochondria [25] and PARP cleavage [26,27], by blocking the lethal DNA damage repair (PLDR) system [28], by inducing G1/S cell cycle arrest [29], and by activating c-JUN NH2-terminal kinase [30] and caspases [31]. Recent data have revealed that NAD(P)H:quinone oxidoreductase (NQO1) is a critical enzyme in bLmediated inhibition of cancer proliferation [23,32].…”

Section: Introductionmentioning

confidence: 99%

NQO1 is Required for Beta-lapachone-mediated Downregulation of Breast Cancer Stem Cell Activity

Kim¹,

Cho²

2018

Preprint

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Background: Cancer stem cells (CSCs) exhibit self-renewal activity and give rise to other cell types in tumors. Due to the infinite proliferative potential of CSCs, drugs targeting these cells are necessary to completely inhibit cancer development. beta-lapachone (bL) has been widely used to treat cancer development, but its effect on cancer stem cells remain elusive. Thus, we investigated the effect of bL on mammosphere formation using breast cancer stem cell (BCSC) marker positive cells, MDA-MB-231. Methods: MDA-MB-231 Cells, which is negative for NQO1 expression, was constructed to stably express NQO1(NQO1 stable cells) to see the effect of bL. The effect of bL on cells were evaluated by wound healing and Transwell cell culture chambers, and ALDEFLUOR assay. Results: Here, we show that bL inhibited the proliferative ability of mammosphere derived from BCSC marker-positive cells, MDA-MB-231, in an NQO1-dependent manner. bL treatment efficiently downregulated expression level of BCSC markers CD44, ALDH1A1, and DLGAP5 that recently identified as a stem cell proliferation marker in both cultured cells and mammosphered cells. Moreover, bL efficiently downregulates cell proliferation and migration activities. Conclusions: These results strongly suggest that bL could be a therapeutic agent targeting breast cancer stem cells with proper NQO1 expression.

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Combinative effects of β-Lapachone and APO866 on pancreatic cancer cell death through reactive oxygen species production and PARP-1 activation

Cited by 16 publications

References 50 publications

Strictly Approximating Attributes of DNA Lesion Repair in Terms of Inherent DNA Responses to Mutability and Malignant Transformation

Strictly Approximating Attributes of DNA Lesion Repair in Terms of Inherent DNA Responses to Mutability and Malignant Transformation

Juglone–ascorbic acid synergy inhibits metastasis and induces apoptotic cell death in poorly differentiated thyroid carcinoma by perturbing SOD and catalase activities

NQO1 is Required for Beta-lapachone-mediated Downregulation of Breast Cancer Stem Cell Activity

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