Anticancer effects of propionic acid inducing cell death in cervical cancer cells

Chau Ha Pham; Joo Eun Lee; Jinha Yu; Sung Hoon Lee; Kyung Rok Yu; Jaewoo Hong; Namki Cho; Seil Kim; Dukjin Kang; Soojin Lee; Hee Min Yoo

doi:10.3390/molecules26164951

Anticancer effects of propionic acid inducing cell death in cervical cancer cells

Chau Ha Pham, Joo Eun Lee, Jinha Yu, Sung Hoon Lee, Kyung Rok Yu, Jaewoo Hong, Namki Cho, Seil Kim, Dukjin Kang, Soojin Lee, Hee Min Yoo

Department of Pharmaceutical Sciences

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

24 Scopus citations

Abstract

Recent studies found that short-chain fatty acids (SCFAs), which are produced through bacterial fermentation in the gastrointestinal tract, have oncoprotective effects against cervical cancer. The most common SCFAs that are well known include acetic acid, butyric acid, and propionic acid, among which propionic acid (PA) has been reported to induce apoptosis in HeLa cells. However, the mechanism in which SCFAs suppress HeLa cell viability remain poorly understood. Our study aims to provide a more detailed look into the mechanism of PA in HeLa cells. Flow cytometry analysis revealed that PA induces reactive oxygen species (ROS), leading to the dysfunction of the mitochondrial membrane. Moreover, PA inhibits NF-κB and AKT/mTOR signaling pathways and induces LC3B protein levels, resulting in autophagy. PA also increased the sub-G1 cell population that is characteristic of cell death. Therefore, the results of this study propose that PA inhibits HeLa cell viability through a mechanism mediated by the induction of autophagy. The study also suggests a new approach for cervical cancer therapeutics.

Original language	English
Article number	4951
Journal	Molecules
Volume	26
Issue number	16
DOIs	https://doi.org/10.3390/molecules26164951
State	Published - 2 Aug 2021

Bibliographical note

Funding Information:
Funding: This research was supported by the “Establishment of measurement standards for Chemistry and Radiation”, grant number KRISS-2021-GP2021-0003 funded by the Korea Research Institute of Standards and Science. In addition, this work was supported by the Ministry of Science and ICT (MSIT), National Research Foundation of Korea (NRF-2019M3A9F3065868), The Ministry of Health and Welfare (MOHW), the Korea Health Industry Development Institute (KHIDI, HI20C0558), the Ministry of Trade, Industry & Energy (MOTIE), and Korea Evaluation Institute of Industrial Technology (KEIT, 20009350). ORCID ID (Hee Min Yoo: 0000-0002-5951-2137; Chau Ha Pham: 0000-0001-6041-3294; Joo-Eun Lee: 0000-0002-2495-1439; Seil Kim: 0000-0003-3465-7118, Dukjin Kang: 0000-0002-5924-9674).

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

Keywords

Cervical cancer
HeLa
Propionic acid
Reactive oxygen species
Short-chain fatty acids

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@article{91e95743e3e74900b7e7495ccec6f820,

title = "Anticancer effects of propionic acid inducing cell death in cervical cancer cells",

abstract = "Recent studies found that short-chain fatty acids (SCFAs), which are produced through bacterial fermentation in the gastrointestinal tract, have oncoprotective effects against cervical cancer. The most common SCFAs that are well known include acetic acid, butyric acid, and propionic acid, among which propionic acid (PA) has been reported to induce apoptosis in HeLa cells. However, the mechanism in which SCFAs suppress HeLa cell viability remain poorly understood. Our study aims to provide a more detailed look into the mechanism of PA in HeLa cells. Flow cytometry analysis revealed that PA induces reactive oxygen species (ROS), leading to the dysfunction of the mitochondrial membrane. Moreover, PA inhibits NF-κB and AKT/mTOR signaling pathways and induces LC3B protein levels, resulting in autophagy. PA also increased the sub-G1 cell population that is characteristic of cell death. Therefore, the results of this study propose that PA inhibits HeLa cell viability through a mechanism mediated by the induction of autophagy. The study also suggests a new approach for cervical cancer therapeutics.",

keywords = "Cervical cancer, HeLa, Propionic acid, Reactive oxygen species, Short-chain fatty acids",

author = "Pham, {Chau Ha} and Lee, {Joo Eun} and Jinha Yu and Lee, {Sung Hoon} and Yu, {Kyung Rok} and Jaewoo Hong and Namki Cho and Seil Kim and Dukjin Kang and Soojin Lee and Yoo, {Hee Min}",

note = "Funding Information: Funding: This research was supported by the “Establishment of measurement standards for Chemistry and Radiation”, grant number KRISS-2021-GP2021-0003 funded by the Korea Research Institute of Standards and Science. In addition, this work was supported by the Ministry of Science and ICT (MSIT), National Research Foundation of Korea (NRF-2019M3A9F3065868), The Ministry of Health and Welfare (MOHW), the Korea Health Industry Development Institute (KHIDI, HI20C0558), the Ministry of Trade, Industry & Energy (MOTIE), and Korea Evaluation Institute of Industrial Technology (KEIT, 20009350). ORCID ID (Hee Min Yoo: 0000-0002-5951-2137; Chau Ha Pham: 0000-0001-6041-3294; Joo-Eun Lee: 0000-0002-2495-1439; Seil Kim: 0000-0003-3465-7118, Dukjin Kang: 0000-0002-5924-9674). Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland.",

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AU - Lee, Joo Eun

AU - Yu, Jinha

AU - Lee, Sung Hoon

AU - Yu, Kyung Rok

AU - Hong, Jaewoo

AU - Cho, Namki

AU - Kim, Seil

AU - Kang, Dukjin

AU - Lee, Soojin

AU - Yoo, Hee Min

N1 - Funding Information: Funding: This research was supported by the “Establishment of measurement standards for Chemistry and Radiation”, grant number KRISS-2021-GP2021-0003 funded by the Korea Research Institute of Standards and Science. In addition, this work was supported by the Ministry of Science and ICT (MSIT), National Research Foundation of Korea (NRF-2019M3A9F3065868), The Ministry of Health and Welfare (MOHW), the Korea Health Industry Development Institute (KHIDI, HI20C0558), the Ministry of Trade, Industry & Energy (MOTIE), and Korea Evaluation Institute of Industrial Technology (KEIT, 20009350). ORCID ID (Hee Min Yoo: 0000-0002-5951-2137; Chau Ha Pham: 0000-0001-6041-3294; Joo-Eun Lee: 0000-0002-2495-1439; Seil Kim: 0000-0003-3465-7118, Dukjin Kang: 0000-0002-5924-9674). Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

PY - 2021/8/2

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N2 - Recent studies found that short-chain fatty acids (SCFAs), which are produced through bacterial fermentation in the gastrointestinal tract, have oncoprotective effects against cervical cancer. The most common SCFAs that are well known include acetic acid, butyric acid, and propionic acid, among which propionic acid (PA) has been reported to induce apoptosis in HeLa cells. However, the mechanism in which SCFAs suppress HeLa cell viability remain poorly understood. Our study aims to provide a more detailed look into the mechanism of PA in HeLa cells. Flow cytometry analysis revealed that PA induces reactive oxygen species (ROS), leading to the dysfunction of the mitochondrial membrane. Moreover, PA inhibits NF-κB and AKT/mTOR signaling pathways and induces LC3B protein levels, resulting in autophagy. PA also increased the sub-G1 cell population that is characteristic of cell death. Therefore, the results of this study propose that PA inhibits HeLa cell viability through a mechanism mediated by the induction of autophagy. The study also suggests a new approach for cervical cancer therapeutics.

AB - Recent studies found that short-chain fatty acids (SCFAs), which are produced through bacterial fermentation in the gastrointestinal tract, have oncoprotective effects against cervical cancer. The most common SCFAs that are well known include acetic acid, butyric acid, and propionic acid, among which propionic acid (PA) has been reported to induce apoptosis in HeLa cells. However, the mechanism in which SCFAs suppress HeLa cell viability remain poorly understood. Our study aims to provide a more detailed look into the mechanism of PA in HeLa cells. Flow cytometry analysis revealed that PA induces reactive oxygen species (ROS), leading to the dysfunction of the mitochondrial membrane. Moreover, PA inhibits NF-κB and AKT/mTOR signaling pathways and induces LC3B protein levels, resulting in autophagy. PA also increased the sub-G1 cell population that is characteristic of cell death. Therefore, the results of this study propose that PA inhibits HeLa cell viability through a mechanism mediated by the induction of autophagy. The study also suggests a new approach for cervical cancer therapeutics.

KW - Cervical cancer

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KW - Propionic acid

KW - Reactive oxygen species

KW - Short-chain fatty acids

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SN - 1420-3049

VL - 26

JO - Molecules

JF - Molecules

IS - 16

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ER -

Anticancer effects of propionic acid inducing cell death in cervical cancer cells

Abstract

Bibliographical note

Keywords

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