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

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-κB. Overall, the results of the present study indicated that K potentiated the anti-tumoral effects of A in breast cancer cells in vitro.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Frajese GV,Benvenuto M,Fantini M,Ambrosin E,Sacchetti P,Masuelli L,Giganti MG,Modesti A,Bei R

doi

10.3892/ol.2016.4506

subject

Has Abstract

pub_date

2016-06-01 00:00:00

pages

4224-4234

issue

6

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-4506

journal_volume

11

pub_type

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