Disruption of endoplasmic reticulum and ros production in human ovarian cancer by campesterol

Hyocheol Bae; Sunwoo Park; Changwon Yang; Gwonhwa Song; Whasun Lim

doi:10.3390/antiox10030379

Disruption of endoplasmic reticulum and ros production in human ovarian cancer by campesterol

Hyocheol Bae, Sunwoo Park, Changwon Yang, Gwonhwa Song, Whasun Lim

Research output: Contribution to journal › Article › peer-review

41 Citations (Scopus)

Abstract

Phytosterols, which are present in a variety of foods, exhibit various physiological functions and do not have any side effects. Here, we attempted to identify functional role of campesterol in regulation of oxidative stress by leading to cell death of ovarian cancer. We investigated the effects of campesterol on cancer cell aggregation using a three‐dimensional (3D) culture of human ovarian cancer cells. The effects of campesterol on apoptosis, protein expression, proliferation, the cell cycle, and the migration of these cells were determined to unravel the underlying mechanism. We also investigated whether campesterol regulates mitochondrial function, the generation of reactive oxygen species (ROS), and calcium concentrations. Our results show that campesterol activates cell death signals and cell death in human ovarian cancer cells. Excessive calcium levels and ROS production were induced by campesterol in the two selected ovarian cancer cell lines. Moreover, campesterol suppressed cell proliferation, cell cycle progression, and cell aggregation in ovarian cancer cells. Campesterol also enhanced the anticancer effects of conventional anticancer agents. The present study shows that campesterol can be used as a novel anticancer drug for human ovarian cancer.

Original language	English
Article number	379
Pages (from-to)	1-18
Number of pages	18
Journal	Antioxidants
Volume	10
Issue number	3
DOIs	https://doi.org/10.3390/antiox10030379
Publication status	Published - 2021 Mar

Bibliographical note

Funding Information:
This research was supported by the National Research Foundation of Korea (NRF) grant, funded by the Ministry of Science and ICT(MSIT), Republic of Korea (grant number: 2019R1A2C2089914) and supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Republic of Korea (grant number: 2020R1I1A1A01067648). Also, this study supported by KMI (Korea Medical Institute), Republic of Korea.

Funding Information:
Funding: This research was supported by the National Research Foundation of Korea (NRF) grant, funded by the Ministry of Science and ICT(MSIT), Republic of Korea (grant number: 2019R1A2C2089914) and supported by Basic Science Research Program through the National Re‐ search Foundation of Korea (NRF) funded by the Ministry of Education, Republic of Korea (grant number: 2020R1I1A1A01067648). Also, this study supported by KMI (Korea Medical Institute), Re‐ public of Korea.

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

Campesterol
Cell death
Mitochondria dysfunction
Ovarian cancer
ROS

ASJC Scopus subject areas

Biochemistry
Physiology
Molecular Biology
Clinical Biochemistry
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3390/antiox10030379

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title = "Disruption of endoplasmic reticulum and ros production in human ovarian cancer by campesterol",

abstract = "Phytosterols, which are present in a variety of foods, exhibit various physiological functions and do not have any side effects. Here, we attempted to identify functional role of campesterol in regulation of oxidative stress by leading to cell death of ovarian cancer. We investigated the effects of campesterol on cancer cell aggregation using a three‐dimensional (3D) culture of human ovarian cancer cells. The effects of campesterol on apoptosis, protein expression, proliferation, the cell cycle, and the migration of these cells were determined to unravel the underlying mechanism. We also investigated whether campesterol regulates mitochondrial function, the generation of reactive oxygen species (ROS), and calcium concentrations. Our results show that campesterol activates cell death signals and cell death in human ovarian cancer cells. Excessive calcium levels and ROS production were induced by campesterol in the two selected ovarian cancer cell lines. Moreover, campesterol suppressed cell proliferation, cell cycle progression, and cell aggregation in ovarian cancer cells. Campesterol also enhanced the anticancer effects of conventional anticancer agents. The present study shows that campesterol can be used as a novel anticancer drug for human ovarian cancer.",

keywords = "Campesterol, Cell death, Mitochondria dysfunction, Ovarian cancer, ROS",

author = "Hyocheol Bae and Sunwoo Park and Changwon Yang and Gwonhwa Song and Whasun Lim",

note = "Funding Information: This research was supported by the National Research Foundation of Korea (NRF) grant, funded by the Ministry of Science and ICT(MSIT), Republic of Korea (grant number: 2019R1A2C2089914) and supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Republic of Korea (grant number: 2020R1I1A1A01067648). Also, this study supported by KMI (Korea Medical Institute), Republic of Korea. Funding Information: Funding: This research was supported by the National Research Foundation of Korea (NRF) grant, funded by the Ministry of Science and ICT(MSIT), Republic of Korea (grant number: 2019R1A2C2089914) and supported by Basic Science Research Program through the National Re‐ search Foundation of Korea (NRF) funded by the Ministry of Education, Republic of Korea (grant number: 2020R1I1A1A01067648). Also, this study supported by KMI (Korea Medical Institute), Re‐ public of Korea. Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2021",

month = mar,

doi = "10.3390/antiox10030379",

language = "English",

volume = "10",

pages = "1--18",

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AU - Bae, Hyocheol

AU - Park, Sunwoo

AU - Yang, Changwon

AU - Song, Gwonhwa

AU - Lim, Whasun

N1 - Funding Information: This research was supported by the National Research Foundation of Korea (NRF) grant, funded by the Ministry of Science and ICT(MSIT), Republic of Korea (grant number: 2019R1A2C2089914) and supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Republic of Korea (grant number: 2020R1I1A1A01067648). Also, this study supported by KMI (Korea Medical Institute), Republic of Korea. Funding Information: Funding: This research was supported by the National Research Foundation of Korea (NRF) grant, funded by the Ministry of Science and ICT(MSIT), Republic of Korea (grant number: 2019R1A2C2089914) and supported by Basic Science Research Program through the National Re‐ search Foundation of Korea (NRF) funded by the Ministry of Education, Republic of Korea (grant number: 2020R1I1A1A01067648). Also, this study supported by KMI (Korea Medical Institute), Re‐ public of Korea. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

PY - 2021/3

Y1 - 2021/3

N2 - Phytosterols, which are present in a variety of foods, exhibit various physiological functions and do not have any side effects. Here, we attempted to identify functional role of campesterol in regulation of oxidative stress by leading to cell death of ovarian cancer. We investigated the effects of campesterol on cancer cell aggregation using a three‐dimensional (3D) culture of human ovarian cancer cells. The effects of campesterol on apoptosis, protein expression, proliferation, the cell cycle, and the migration of these cells were determined to unravel the underlying mechanism. We also investigated whether campesterol regulates mitochondrial function, the generation of reactive oxygen species (ROS), and calcium concentrations. Our results show that campesterol activates cell death signals and cell death in human ovarian cancer cells. Excessive calcium levels and ROS production were induced by campesterol in the two selected ovarian cancer cell lines. Moreover, campesterol suppressed cell proliferation, cell cycle progression, and cell aggregation in ovarian cancer cells. Campesterol also enhanced the anticancer effects of conventional anticancer agents. The present study shows that campesterol can be used as a novel anticancer drug for human ovarian cancer.

AB - Phytosterols, which are present in a variety of foods, exhibit various physiological functions and do not have any side effects. Here, we attempted to identify functional role of campesterol in regulation of oxidative stress by leading to cell death of ovarian cancer. We investigated the effects of campesterol on cancer cell aggregation using a three‐dimensional (3D) culture of human ovarian cancer cells. The effects of campesterol on apoptosis, protein expression, proliferation, the cell cycle, and the migration of these cells were determined to unravel the underlying mechanism. We also investigated whether campesterol regulates mitochondrial function, the generation of reactive oxygen species (ROS), and calcium concentrations. Our results show that campesterol activates cell death signals and cell death in human ovarian cancer cells. Excessive calcium levels and ROS production were induced by campesterol in the two selected ovarian cancer cell lines. Moreover, campesterol suppressed cell proliferation, cell cycle progression, and cell aggregation in ovarian cancer cells. Campesterol also enhanced the anticancer effects of conventional anticancer agents. The present study shows that campesterol can be used as a novel anticancer drug for human ovarian cancer.

KW - Campesterol

KW - Cell death

KW - Mitochondria dysfunction

KW - Ovarian cancer

KW - ROS

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DO - 10.3390/antiox10030379

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VL - 10

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JO - Antioxidants

JF - Antioxidants

IS - 3

M1 - 379

ER -

Disruption of endoplasmic reticulum and ros production in human ovarian cancer by campesterol

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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