Cargando…

Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage

Cervical cancer is a health problem among women worldwide. Considering the limitations of prevention and antineoplastic chemotherapy against cervical cancer, research is needed to discover new, more effective, and safe antitumor agents. In the present study, we investigated the in vitro cytotoxicity...

Descripción completa

Detalles Bibliográficos
Autores principales: Zani, Aline Pinto, Zani, Caroline Pinto, Din, Zia Ud, Rodrigues-Filho, Edson, Ueda-Nakamura, Tânia, Garcia, Francielle Pelegrin, de Oliveira Silva, Sueli, Nakamura, Celso Vataru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952489/
https://www.ncbi.nlm.nih.gov/pubmed/36829876
http://dx.doi.org/10.3390/antiox12020317
_version_ 1784893644158795776
author Zani, Aline Pinto
Zani, Caroline Pinto
Din, Zia Ud
Rodrigues-Filho, Edson
Ueda-Nakamura, Tânia
Garcia, Francielle Pelegrin
de Oliveira Silva, Sueli
Nakamura, Celso Vataru
author_facet Zani, Aline Pinto
Zani, Caroline Pinto
Din, Zia Ud
Rodrigues-Filho, Edson
Ueda-Nakamura, Tânia
Garcia, Francielle Pelegrin
de Oliveira Silva, Sueli
Nakamura, Celso Vataru
author_sort Zani, Aline Pinto
collection PubMed
description Cervical cancer is a health problem among women worldwide. Considering the limitations of prevention and antineoplastic chemotherapy against cervical cancer, research is needed to discover new, more effective, and safe antitumor agents. In the present study, we investigated the in vitro cytotoxicity of a new synthetic dibenzylideneacetone derived from 1,5-diaryl-3-oxo-1,4-pentadienyl (A3K2A3) against cervical cancer cells immortalized by HPV 16 (SiHa), and 18 (HeLa) by MTT assay. Furthermore, we performed spectrofluorimetry, flow cytometry, and Western blot analyzes to explore the inhibitory mechanism of A3K2A3 in cervical cancer cells. A3K2A3 showed cytotoxic activity against both cell lines. Mitochondrial depolarization and reduction in intracellular ATP levels were observed, which may be dependent on the redox imbalance between increased ROS and reduced levels of the antioxidant defense. In addition, damage to the cell membrane and DNA, and effective blocking of cell division in the G2/M phase were detected, which possibly led to the induction of apoptosis. This result was further confirmed by the upregulation of apoptosis-related proteins Bax, cytochrome C, and caspases 9 and 3. Our results provided the first evidence that A3K2A3 contributes to the suppression of cervical cancer in vitro, showing promise as a possible alternative for the treatment of this cancer.
format Online
Article
Text
id pubmed-9952489
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-99524892023-02-25 Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage Zani, Aline Pinto Zani, Caroline Pinto Din, Zia Ud Rodrigues-Filho, Edson Ueda-Nakamura, Tânia Garcia, Francielle Pelegrin de Oliveira Silva, Sueli Nakamura, Celso Vataru Antioxidants (Basel) Article Cervical cancer is a health problem among women worldwide. Considering the limitations of prevention and antineoplastic chemotherapy against cervical cancer, research is needed to discover new, more effective, and safe antitumor agents. In the present study, we investigated the in vitro cytotoxicity of a new synthetic dibenzylideneacetone derived from 1,5-diaryl-3-oxo-1,4-pentadienyl (A3K2A3) against cervical cancer cells immortalized by HPV 16 (SiHa), and 18 (HeLa) by MTT assay. Furthermore, we performed spectrofluorimetry, flow cytometry, and Western blot analyzes to explore the inhibitory mechanism of A3K2A3 in cervical cancer cells. A3K2A3 showed cytotoxic activity against both cell lines. Mitochondrial depolarization and reduction in intracellular ATP levels were observed, which may be dependent on the redox imbalance between increased ROS and reduced levels of the antioxidant defense. In addition, damage to the cell membrane and DNA, and effective blocking of cell division in the G2/M phase were detected, which possibly led to the induction of apoptosis. This result was further confirmed by the upregulation of apoptosis-related proteins Bax, cytochrome C, and caspases 9 and 3. Our results provided the first evidence that A3K2A3 contributes to the suppression of cervical cancer in vitro, showing promise as a possible alternative for the treatment of this cancer. MDPI 2023-01-30 /pmc/articles/PMC9952489/ /pubmed/36829876 http://dx.doi.org/10.3390/antiox12020317 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zani, Aline Pinto
Zani, Caroline Pinto
Din, Zia Ud
Rodrigues-Filho, Edson
Ueda-Nakamura, Tânia
Garcia, Francielle Pelegrin
de Oliveira Silva, Sueli
Nakamura, Celso Vataru
Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage
title Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage
title_full Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage
title_fullStr Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage
title_full_unstemmed Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage
title_short Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage
title_sort dibenzylideneacetone induces apoptosis in cervical cancer cells through ros-mediated mitochondrial damage
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952489/
https://www.ncbi.nlm.nih.gov/pubmed/36829876
http://dx.doi.org/10.3390/antiox12020317
work_keys_str_mv AT zanialinepinto dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT zanicarolinepinto dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT dinziaud dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT rodriguesfilhoedson dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT uedanakamuratania dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT garciafranciellepelegrin dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT deoliveirasilvasueli dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage
AT nakamuracelsovataru dibenzylideneacetoneinducesapoptosisincervicalcancercellsthroughrosmediatedmitochondrialdamage