Introduction: The combination chemotherapies with methotrexate plus vinblastine, doxorubicin and cisplatin are often ineffective against bladder cancer [1]. Alternative regimens based on new anticancer compounds are therefore needed to overcome conventional drug resistance and optimize patients’ outcome. It has already been demonstrated that phytochemicals extracted from Beta vulgaris cicla (vitexin-2-O-xyloside) and Beta vulgaris rubra (betaxanthins and betacyanins) possess chemopreventive properties [2]. Cancer microen-vironment is pro-oxidant and pro-inflammatory and all those compounds able to worsen these conditions could fight cancer.Materials and methods: T24 bladder cancer cells were grown in complete DMEM and Sulforhodamine B as-say was performed to evaluate the cytotoxicity of vitexin-2-O-xyloside (VOX) and betalains (BLS) on cancer cells. COX-2 activity was evaluated on the samples of cytosol extracted from T24 cells by a spectrophotome-tric assay through the values of absorbance at 590 nm. Results: We tested VOX and BLS on T24 human bladder carcinoma cell line and we evaluated their cytotoxi-city in time-course experiments. We incubated T24 cells with individual compounds and their combinations for 24, 48 and 72h. We demonstrated that VOX and BLS, alone or in combination, are able to kill T24 cells, showing a synergistic effect after 48h treatment. We than evaluated the activity of COX-2, a key pro-inflam-matory enzyme, in the cytosol of T24 cells, which was incubated with VOX. We found an increase of the COX-2 activity in the presence of VOX, thus indicating a pro-inflammatory effect of this drug. Discussion: A mixture of VOX and BLS is able to kill efficiently chemoresistant T24 bladder cancer cells. These data underlie the importance of cocktails of phytochemicals in the therapy of human cancers that are resistant to conventional drugs. Molecular studies are in progress to detect the cellular network of signaling involved in this cytotoxic effect.

Natural extracts from the genus Beta and their cytotoxic activity on T24 human bladder cancer cells

NINFALI, PAOLINO
2015

Abstract

Introduction: The combination chemotherapies with methotrexate plus vinblastine, doxorubicin and cisplatin are often ineffective against bladder cancer [1]. Alternative regimens based on new anticancer compounds are therefore needed to overcome conventional drug resistance and optimize patients’ outcome. It has already been demonstrated that phytochemicals extracted from Beta vulgaris cicla (vitexin-2-O-xyloside) and Beta vulgaris rubra (betaxanthins and betacyanins) possess chemopreventive properties [2]. Cancer microen-vironment is pro-oxidant and pro-inflammatory and all those compounds able to worsen these conditions could fight cancer.Materials and methods: T24 bladder cancer cells were grown in complete DMEM and Sulforhodamine B as-say was performed to evaluate the cytotoxicity of vitexin-2-O-xyloside (VOX) and betalains (BLS) on cancer cells. COX-2 activity was evaluated on the samples of cytosol extracted from T24 cells by a spectrophotome-tric assay through the values of absorbance at 590 nm. Results: We tested VOX and BLS on T24 human bladder carcinoma cell line and we evaluated their cytotoxi-city in time-course experiments. We incubated T24 cells with individual compounds and their combinations for 24, 48 and 72h. We demonstrated that VOX and BLS, alone or in combination, are able to kill T24 cells, showing a synergistic effect after 48h treatment. We than evaluated the activity of COX-2, a key pro-inflam-matory enzyme, in the cytosol of T24 cells, which was incubated with VOX. We found an increase of the COX-2 activity in the presence of VOX, thus indicating a pro-inflammatory effect of this drug. Discussion: A mixture of VOX and BLS is able to kill efficiently chemoresistant T24 bladder cancer cells. These data underlie the importance of cocktails of phytochemicals in the therapy of human cancers that are resistant to conventional drugs. Molecular studies are in progress to detect the cellular network of signaling involved in this cytotoxic effect.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11576/2629226
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