University of Hertfordshire

From the same journal

By the same authors

Standard

Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells. / Vazhappilly, Cijo George; Hodeify, Rawad; Siddiqui, Shoib Sarwar; Laham, Amina Jamal; Menon, Varsha; El-Awady, Raafat; Matar, Rachel; Merheb, Maxime; Marton, John; Al Zouabi, Hussain Abdel Karim; Radhakrishnan, Rajan.

In: Phytotherapy Research, 07.12.2020.

Research output: Contribution to journalArticlepeer-review

Harvard

Vazhappilly, CG, Hodeify, R, Siddiqui, SS, Laham, AJ, Menon, V, El-Awady, R, Matar, R, Merheb, M, Marton, J, Al Zouabi, HAK & Radhakrishnan, R 2020, 'Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells', Phytotherapy Research. https://doi.org/10.1002/ptr.6970

APA

Vazhappilly, C. G., Hodeify, R., Siddiqui, S. S., Laham, A. J., Menon, V., El-Awady, R., Matar, R., Merheb, M., Marton, J., Al Zouabi, H. A. K., & Radhakrishnan, R. (2020). Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells. Phytotherapy Research. https://doi.org/10.1002/ptr.6970

Vancouver

Author

Vazhappilly, Cijo George ; Hodeify, Rawad ; Siddiqui, Shoib Sarwar ; Laham, Amina Jamal ; Menon, Varsha ; El-Awady, Raafat ; Matar, Rachel ; Merheb, Maxime ; Marton, John ; Al Zouabi, Hussain Abdel Karim ; Radhakrishnan, Rajan. / Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells. In: Phytotherapy Research. 2020.

Bibtex

@article{9325100aea3c4eb89334523d29128d4c,
title = "Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells",
abstract = "Targeting cell cycle and inducing DNA damage by activating cell death pathways are considered as effective therapeutic strategy for combating breast cancer progression. Many of the naturally known small molecules target these signaling pathways and are effective against resistant and/or aggressive types of breast cancers. Here, we investigated the effect of catechol, a naturally occurring plant compound, for its specificity and chemotherapeutic efficacies in breast cancer (MCF-7 and MDA-MB-231) cells. Catechol treatment showed concentration-dependent cytotoxicity and antiproliferative growth in both MCF-7 and MDA-MB-231 cells while sparing minimal effects on noncancerous (F-180 and HK2) cells. Catechol modulated differential DNA damage effects by activating ATM/ATR pathways and showed enhanced γ-H2AX expression, as an indicator for DNA double-stranded breaks. MCF-7 cells showed G1 cell cycle arrest by regulating p21-mediated cyclin E/Cdk2 inhibition. Furthermore, activation of p53 triggered a caspase-mediated cell death mechanism by inhibiting regulatory proteins such as DNMT1, p-BRCA1, MCL-1, and PDCD6 with an increased Bax/Bcl-2 ratio. Overall, our results showed that catechol possesses favorable safety profile for noncancerous cells while specifically targeting multiple signaling cascades to inhibit proliferation in breast cancer cells.",
author = "Vazhappilly, {Cijo George} and Rawad Hodeify and Siddiqui, {Shoib Sarwar} and Laham, {Amina Jamal} and Varsha Menon and Raafat El-Awady and Rachel Matar and Maxime Merheb and John Marton and {Al Zouabi}, {Hussain Abdel Karim} and Rajan Radhakrishnan",
note = "{\textcopyright} 2020 John Wiley & Sons, Ltd.",
year = "2020",
month = dec,
day = "7",
doi = "10.1002/ptr.6970",
language = "English",
journal = "Phytotherapy Research",
issn = "0951-418X",
publisher = "John Wiley and Sons Ltd",

}

RIS

TY - JOUR

T1 - Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells

AU - Vazhappilly, Cijo George

AU - Hodeify, Rawad

AU - Siddiqui, Shoib Sarwar

AU - Laham, Amina Jamal

AU - Menon, Varsha

AU - El-Awady, Raafat

AU - Matar, Rachel

AU - Merheb, Maxime

AU - Marton, John

AU - Al Zouabi, Hussain Abdel Karim

AU - Radhakrishnan, Rajan

N1 - © 2020 John Wiley & Sons, Ltd.

PY - 2020/12/7

Y1 - 2020/12/7

N2 - Targeting cell cycle and inducing DNA damage by activating cell death pathways are considered as effective therapeutic strategy for combating breast cancer progression. Many of the naturally known small molecules target these signaling pathways and are effective against resistant and/or aggressive types of breast cancers. Here, we investigated the effect of catechol, a naturally occurring plant compound, for its specificity and chemotherapeutic efficacies in breast cancer (MCF-7 and MDA-MB-231) cells. Catechol treatment showed concentration-dependent cytotoxicity and antiproliferative growth in both MCF-7 and MDA-MB-231 cells while sparing minimal effects on noncancerous (F-180 and HK2) cells. Catechol modulated differential DNA damage effects by activating ATM/ATR pathways and showed enhanced γ-H2AX expression, as an indicator for DNA double-stranded breaks. MCF-7 cells showed G1 cell cycle arrest by regulating p21-mediated cyclin E/Cdk2 inhibition. Furthermore, activation of p53 triggered a caspase-mediated cell death mechanism by inhibiting regulatory proteins such as DNMT1, p-BRCA1, MCL-1, and PDCD6 with an increased Bax/Bcl-2 ratio. Overall, our results showed that catechol possesses favorable safety profile for noncancerous cells while specifically targeting multiple signaling cascades to inhibit proliferation in breast cancer cells.

AB - Targeting cell cycle and inducing DNA damage by activating cell death pathways are considered as effective therapeutic strategy for combating breast cancer progression. Many of the naturally known small molecules target these signaling pathways and are effective against resistant and/or aggressive types of breast cancers. Here, we investigated the effect of catechol, a naturally occurring plant compound, for its specificity and chemotherapeutic efficacies in breast cancer (MCF-7 and MDA-MB-231) cells. Catechol treatment showed concentration-dependent cytotoxicity and antiproliferative growth in both MCF-7 and MDA-MB-231 cells while sparing minimal effects on noncancerous (F-180 and HK2) cells. Catechol modulated differential DNA damage effects by activating ATM/ATR pathways and showed enhanced γ-H2AX expression, as an indicator for DNA double-stranded breaks. MCF-7 cells showed G1 cell cycle arrest by regulating p21-mediated cyclin E/Cdk2 inhibition. Furthermore, activation of p53 triggered a caspase-mediated cell death mechanism by inhibiting regulatory proteins such as DNMT1, p-BRCA1, MCL-1, and PDCD6 with an increased Bax/Bcl-2 ratio. Overall, our results showed that catechol possesses favorable safety profile for noncancerous cells while specifically targeting multiple signaling cascades to inhibit proliferation in breast cancer cells.

U2 - 10.1002/ptr.6970

DO - 10.1002/ptr.6970

M3 - Article

C2 - 33289235

JO - Phytotherapy Research

JF - Phytotherapy Research

SN - 0951-418X

ER -