Roe Protein Hydrolysates of Giant Grouper (Epinephelus lanceolatus) Inhibit Cell Proliferation of Oral Cancer Cells Involving Apoptosis and Oxidative Stress

Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH...

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Published inBioMed research international Vol. 2016; no. 2016; pp. 1 - 12
Main Authors Chang, Hsueh-Wei, Lee, Sheng-Yang, Wang, Hui-Ru, Liu, Ya-Sin, Tang, Jen-Yang, Yang, Jing-Iong, Yen, Ching-Yu
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 01.01.2016
John Wiley & Sons, Inc
Subjects
Algae
Animals
Antioxidants
Antioxidants - metabolism
Apoptosis
Breast cancer
Cancer
Cancer cells
Cancer therapies
Care and treatment
Cell Cycle
Cell growth
Cell Line, Tumor - drug effects
Cell Proliferation
Cell Survival
Dose-Response Relationship, Drug
Drug dosages
Epinephelus lanceolatus
Fish
Fish Proteins - pharmacology
Hospitals
Humans
Hydrolysis
Membrane Potential, Mitochondrial
Mouth cancer
Mouth Neoplasms - pathology
Oncology
Oncology, Experimental
Oral cancer
Ovum - chemistry
Oxidative Stress
Perciformes
Protein hydrolysates
Protein Hydrolysates - pharmacology
Proteins
Reactive Oxygen Species - metabolism
Science
Seafood
Superoxide
Superoxides - metabolism
Ultrafiltration
Taiwan
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Abstract Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.
AbstractList Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.
Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper (Epinephelus lanceolatus) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.
Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study, we firstly used the ultrafiltrated roe hydrolysates (URH) derived from giant grouper ( Epinephelus lanceolatus ) to evaluate the impact of URH on proliferation against oral cancer cells. We found that URH dose-responsively reduced cell viability of two oral cancer cells (Ca9-22 and CAL 27) in terms of ATP assay. Using flow cytometry, URH-induced apoptosis of Ca9-22 cells was validated by morphological features of apoptosis, sub-G1 accumulation, and annexin V staining in dose-responsive manners. URH also induced oxidative stress in Ca9-22 cells in terms of reactive oxygen species (ROS)/superoxide generations and mitochondrial depolarization. Taken together, these data suggest that URH is a potential natural product for antioral cancer therapy.
Audience Academic
Author Tang, Jen-Yang
Yen, Ching-Yu
Chang, Hsueh-Wei
Lee, Sheng-Yang
Yang, Jing-Iong
Wang, Hui-Ru
Liu, Ya-Sin
AuthorAffiliation 1 Department of Seafood Science, National Kaohsiung Marine University, Kaohsiung 81157, Taiwan
5 Department of Biomedical Science and Environmental Biology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
2 Department of Radiation Oncology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
6 School of Dentistry, Taipei Medical University, Taipei 11031, Taiwan
11 Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
7 Division of Orthodontics, Wan-Fang Medical Center, Taipei Medical University, Taipei 11648, Taiwan
10 Center for Research Resources and Development of Kaohsiung Medical University, Kaohsiung 80708, Taiwan
9 Institute of Medical Science and Technology, National Sun Yat-sen University, Kaohsiung 80424, Taiwan
3 Department of Radiation Oncology, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan
4 Department of Radiation Oncology, Kaohsiung Municipal Ta-Tung Hospital,
AuthorAffiliation_xml – name: 5 Department of Biomedical Science and Environmental Biology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
– name: 4 Department of Radiation Oncology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung 80708, Taiwan
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– name: 1 Department of Seafood Science, National Kaohsiung Marine University, Kaohsiung 81157, Taiwan
– name: 3 Department of Radiation Oncology, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan
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ContentType Journal Article
Copyright Copyright © 2016 Jing-Iong Yang et al.
COPYRIGHT 2016 John Wiley & Sons, Inc.
Copyright © 2016 Jing-Iong Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright © 2016 Jing-Iong Yang et al. 2016
Copyright_xml – notice: Copyright © 2016 Jing-Iong Yang et al.
– notice: COPYRIGHT 2016 John Wiley & Sons, Inc.
– notice: Copyright © 2016 Jing-Iong Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Snippet Roe protein hydrolysates were reported to have antioxidant property but the anticancer effects were less addressed, especially for oral cancer. In this study,...
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StartPage 1
SubjectTerms Algae
Animals
Antioxidants
Antioxidants - metabolism
Apoptosis
Breast cancer
Cancer
Cancer cells
Cancer therapies
Care and treatment
Cell Cycle
Cell growth
Cell Line, Tumor - drug effects
Cell Proliferation
Cell Survival
Dose-Response Relationship, Drug
Drug dosages
Epinephelus lanceolatus
Fish
Fish Proteins - pharmacology
Hospitals
Humans
Hydrolysis
Membrane Potential, Mitochondrial
Mouth cancer
Mouth Neoplasms - pathology
Oncology
Oncology, Experimental
Oral cancer
Ovum - chemistry
Oxidative Stress
Perciformes
Protein hydrolysates
Protein Hydrolysates - pharmacology
Proteins
Reactive Oxygen Species - metabolism
Science
Seafood
Superoxide
Superoxides - metabolism
Ultrafiltration
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Title Roe Protein Hydrolysates of Giant Grouper (Epinephelus lanceolatus) Inhibit Cell Proliferation of Oral Cancer Cells Involving Apoptosis and Oxidative Stress
URI https://search.emarefa.net/detail/BIM-1099024
https://dx.doi.org/10.1155/2016/8305073
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Volume 2016
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