Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration
Breast cancer is the most common malignant tumor in women, and its incidence is increasing each year. To effectively treat breast cancer, it is important to identify genes involved in its occurrence and development and to exploit them as potential drug therapy targets. Here, we found that potassium...
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Frontiers Media S.A.
2021-06-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2021.616784/full |
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| author | Xiangchan Hou Xiangchan Hou Le Tang Xiayu Li Fang Xiong Yongzhen Mo Xianjie Jiang Xiangying Deng Miao Peng Pan Wu Mengyao Zhao Jiawei Ouyang Lei Shi Yi He Qijia Yan Shanshan Zhang Zhaojian Gong Guiyuan Li Zhaoyang Zeng Fuyan Wang Can Guo Can Guo Wei Xiong Wei Xiong Wei Xiong |
| author_facet | Xiangchan Hou Xiangchan Hou Le Tang Xiayu Li Fang Xiong Yongzhen Mo Xianjie Jiang Xiangying Deng Miao Peng Pan Wu Mengyao Zhao Jiawei Ouyang Lei Shi Yi He Qijia Yan Shanshan Zhang Zhaojian Gong Guiyuan Li Zhaoyang Zeng Fuyan Wang Can Guo Can Guo Wei Xiong Wei Xiong Wei Xiong |
| author_sort | Xiangchan Hou |
| collection | DOAJ |
| description | Breast cancer is the most common malignant tumor in women, and its incidence is increasing each year. To effectively treat breast cancer, it is important to identify genes involved in its occurrence and development and to exploit them as potential drug therapy targets. Here, we found that potassium channel subfamily K member 6 (KCNK6) is significantly overexpressed in breast cancer, however, its function in tumors has not been reported. We further verified that KCNK6 expression is upregulated in breast cancer biopsies. Moreover, overexpressed KCNK6 was found to enhance the proliferation, invasion, and migration ability of breast cancer cells. These effects may occur by weakening cell adhesion and reducing cell hardness, thus affecting the malignant phenotype of breast cancer cells. Our study confirmed, for the first time, that increased KCNK6 expression in breast cancer cells may promote their proliferation, invasion, and migration. Moreover, considering that ion channels serve as therapeutic targets for many small molecular drugs in clinical treatment, targeting KCNK6 may represent a novel strategy for breast cancer therapies. Hence, the results of this study provide a theoretical basis for KCNK6 to become a potential molecular target for breast cancer treatment in the future. |
| first_indexed | 2024-12-21T01:40:54Z |
| format | Article |
| id | doaj.art-334b0e13b74143bc8dbbb6d7c91a4d01 |
| institution | Directory Open Access Journal |
| issn | 2296-634X |
| language | English |
| last_indexed | 2024-12-21T01:40:54Z |
| publishDate | 2021-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj.art-334b0e13b74143bc8dbbb6d7c91a4d012022-12-21T19:20:09ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-06-01910.3389/fcell.2021.616784616784Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and MigrationXiangchan Hou0Xiangchan Hou1Le Tang2Xiayu Li3Fang Xiong4Yongzhen Mo5Xianjie Jiang6Xiangying Deng7Miao Peng8Pan Wu9Mengyao Zhao10Jiawei Ouyang11Lei Shi12Yi He13Qijia Yan14Shanshan Zhang15Zhaojian Gong16Guiyuan Li17Zhaoyang Zeng18Fuyan Wang19Can Guo20Can Guo21Wei Xiong22Wei Xiong23Wei Xiong24NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaHunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, The Third Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Stomatology, Xiangya Hospital, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaDepartment of Oral and Maxillofacial Surgery, The Second Xiangya Hospital, Central South University, Changsha, ChinaNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, ChinaDepartment of Stomatology, Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Stomatology, Xiangya Hospital, Central South University, Changsha, ChinaDepartment of Oral and Maxillofacial Surgery, The Second Xiangya Hospital, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, ChinaKey Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, ChinaHunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, The Third Xiangya Hospital, Central South University, Changsha, ChinaBreast cancer is the most common malignant tumor in women, and its incidence is increasing each year. To effectively treat breast cancer, it is important to identify genes involved in its occurrence and development and to exploit them as potential drug therapy targets. Here, we found that potassium channel subfamily K member 6 (KCNK6) is significantly overexpressed in breast cancer, however, its function in tumors has not been reported. We further verified that KCNK6 expression is upregulated in breast cancer biopsies. Moreover, overexpressed KCNK6 was found to enhance the proliferation, invasion, and migration ability of breast cancer cells. These effects may occur by weakening cell adhesion and reducing cell hardness, thus affecting the malignant phenotype of breast cancer cells. Our study confirmed, for the first time, that increased KCNK6 expression in breast cancer cells may promote their proliferation, invasion, and migration. Moreover, considering that ion channels serve as therapeutic targets for many small molecular drugs in clinical treatment, targeting KCNK6 may represent a novel strategy for breast cancer therapies. Hence, the results of this study provide a theoretical basis for KCNK6 to become a potential molecular target for breast cancer treatment in the future.https://www.frontiersin.org/articles/10.3389/fcell.2021.616784/fullbreast cancerpotassium channelKCNK6proliferationinvasionmigration |
| spellingShingle | Xiangchan Hou Xiangchan Hou Le Tang Xiayu Li Fang Xiong Yongzhen Mo Xianjie Jiang Xiangying Deng Miao Peng Pan Wu Mengyao Zhao Jiawei Ouyang Lei Shi Yi He Qijia Yan Shanshan Zhang Zhaojian Gong Guiyuan Li Zhaoyang Zeng Fuyan Wang Can Guo Can Guo Wei Xiong Wei Xiong Wei Xiong Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration Frontiers in Cell and Developmental Biology breast cancer potassium channel KCNK6 proliferation invasion migration |
| title | Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration |
| title_full | Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration |
| title_fullStr | Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration |
| title_full_unstemmed | Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration |
| title_short | Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration |
| title_sort | potassium channel protein kcnk6 promotes breast cancer cell proliferation invasion and migration |
| topic | breast cancer potassium channel KCNK6 proliferation invasion migration |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2021.616784/full |
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