Ascorbic acid (A) has been demonstrated to exhibit anti-cancer activity in association with chemotherapeutic agents. Potassium (K) is a regulator of cellular proliferation. In the present study, the biological effects of A and K bicarbonate, alone or in combination (A+K), on breast cancer cell lines were evaluated. The survival of cancer cells was determined by sulforhodamine B cell proliferation assay, while analysis of the cell cycle distribution was conducted via fluorescence-activated cell sorting. In addition, the expression of signaling proteins was analyzed upon treatment. The results indicated that there was a heterogeneous response of the different cell lines to A and K, and the best effects were achieved by A+K and A treatment. The interaction between A+K indicated an additive or synergistic effect. In addition, A+K increased the percentage of cells in the sub-G1 phase of the cell cycle, and was the most effective treatment in activating the degradation of poly(adenosine diphosphate-ribose) polymerase-1. In the breast cancer cell line MCF-7, A+K induced the appearance of the 18 kDa isoform of B-cell lymphoma-2-associated X protein (Bax), which is a more potent inducer of apoptosis than the full-length Bax-p21. The effects of A and K on the phosphorylation of extracellular signal-regulated kinase (ERK) 1 and ERK2 were heterogeneous. In addition, treatment with K, A and A+K inhibited the expression of nuclear factor-kappa B. Overall, the results of the present study indicated that K potentiated the anti-tumoral effects of A in breast cancer cells in vitro.

Potassium increases the antitumor effects of ascorbic acid in breast cancer cell lines in vitro / Frajese, Giovanni Vanni; Benvenuto, Monica; Fantini, Massimo; Ambrosin, Elena; Sacchetti, Pamela; Masuelli, Laura; Giganti, Maria Gabriella; Modesti, Andrea; Bei, Roberto. - In: ONCOLOGY LETTERS. - ISSN 1792-1074. - STAMPA. - 11:6(2016), pp. 4224-4234. [10.3892/ol.2016.4506]

Potassium increases the antitumor effects of ascorbic acid in breast cancer cell lines in vitro

MASUELLI, Laura;
2016

Abstract

Ascorbic acid (A) has been demonstrated to exhibit anti-cancer activity in association with chemotherapeutic agents. Potassium (K) is a regulator of cellular proliferation. In the present study, the biological effects of A and K bicarbonate, alone or in combination (A+K), on breast cancer cell lines were evaluated. The survival of cancer cells was determined by sulforhodamine B cell proliferation assay, while analysis of the cell cycle distribution was conducted via fluorescence-activated cell sorting. In addition, the expression of signaling proteins was analyzed upon treatment. The results indicated that there was a heterogeneous response of the different cell lines to A and K, and the best effects were achieved by A+K and A treatment. The interaction between A+K indicated an additive or synergistic effect. In addition, A+K increased the percentage of cells in the sub-G1 phase of the cell cycle, and was the most effective treatment in activating the degradation of poly(adenosine diphosphate-ribose) polymerase-1. In the breast cancer cell line MCF-7, A+K induced the appearance of the 18 kDa isoform of B-cell lymphoma-2-associated X protein (Bax), which is a more potent inducer of apoptosis than the full-length Bax-p21. The effects of A and K on the phosphorylation of extracellular signal-regulated kinase (ERK) 1 and ERK2 were heterogeneous. In addition, treatment with K, A and A+K inhibited the expression of nuclear factor-kappa B. Overall, the results of the present study indicated that K potentiated the anti-tumoral effects of A in breast cancer cells in vitro.
2016
Apoptosis; Ascorbic acid; Breast cancer; Potassium; Oncology; Cancer Research
01 Pubblicazione su rivista::01a Articolo in rivista
Potassium increases the antitumor effects of ascorbic acid in breast cancer cell lines in vitro / Frajese, Giovanni Vanni; Benvenuto, Monica; Fantini, Massimo; Ambrosin, Elena; Sacchetti, Pamela; Masuelli, Laura; Giganti, Maria Gabriella; Modesti, Andrea; Bei, Roberto. - In: ONCOLOGY LETTERS. - ISSN 1792-1074. - STAMPA. - 11:6(2016), pp. 4224-4234. [10.3892/ol.2016.4506]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/905812
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