TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target
Depletion of tribbles pseudokinase 3 (TRIB3) is known to suppress the expression of several tumor-promoting factors, including EGFR. Here, the authors show that TRIB3 interacts with EGFR and regulates its stability and activity, and perturbing EGFR-TRIB3 interaction attenuates NSCLC progression by a...
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Nature Publishing Group
2020-07-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-020-17385-0 |
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doaj-dd56caddb5794e359d42000db61b74592021-07-25T11:40:06ZengNature Publishing GroupNature Communications2041-17232020-07-0111111610.1038/s41467-020-17385-0TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic targetJiao-jiao Yu0Dan-dan Zhou1Xiao-xiao Yang2Bing Cui3Feng-wei Tan4Junjian Wang5Ke Li6Shuang Shang7Cheng Zhang8Xiao-xi Lv9Xiao-wei Zhang10Shan-shan Liu11Jin-mei Yu12Feng Wang13Bo Huang14Fang Hua15Zhuo-Wei Hu16State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeDepartment of Medicinal Synthesis Chemistry, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeDepartment of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical CollegeSchool of Pharmaceutical Sciences, Sun Yat-sen UniversityInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeInstitute of Basic Medicine, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical CollegeDepletion of tribbles pseudokinase 3 (TRIB3) is known to suppress the expression of several tumor-promoting factors, including EGFR. Here, the authors show that TRIB3 interacts with EGFR and regulates its stability and activity, and perturbing EGFR-TRIB3 interaction attenuates NSCLC progression by accelerating EGFR degradation.https://doi.org/10.1038/s41467-020-17385-0 |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Jiao-jiao Yu Dan-dan Zhou Xiao-xiao Yang Bing Cui Feng-wei Tan Junjian Wang Ke Li Shuang Shang Cheng Zhang Xiao-xi Lv Xiao-wei Zhang Shan-shan Liu Jin-mei Yu Feng Wang Bo Huang Fang Hua Zhuo-Wei Hu |
| spellingShingle |
Jiao-jiao Yu Dan-dan Zhou Xiao-xiao Yang Bing Cui Feng-wei Tan Junjian Wang Ke Li Shuang Shang Cheng Zhang Xiao-xi Lv Xiao-wei Zhang Shan-shan Liu Jin-mei Yu Feng Wang Bo Huang Fang Hua Zhuo-Wei Hu TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target Nature Communications |
| author_facet |
Jiao-jiao Yu Dan-dan Zhou Xiao-xiao Yang Bing Cui Feng-wei Tan Junjian Wang Ke Li Shuang Shang Cheng Zhang Xiao-xi Lv Xiao-wei Zhang Shan-shan Liu Jin-mei Yu Feng Wang Bo Huang Fang Hua Zhuo-Wei Hu |
| author_sort |
Jiao-jiao Yu |
| title |
TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target |
| title_short |
TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target |
| title_full |
TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target |
| title_fullStr |
TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target |
| title_full_unstemmed |
TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target |
| title_sort |
trib3-egfr interaction promotes lung cancer progression and defines a therapeutic target |
| publisher |
Nature Publishing Group |
| series |
Nature Communications |
| issn |
2041-1723 |
| publishDate |
2020-07-01 |
| description |
Depletion of tribbles pseudokinase 3 (TRIB3) is known to suppress the expression of several tumor-promoting factors, including EGFR. Here, the authors show that TRIB3 interacts with EGFR and regulates its stability and activity, and perturbing EGFR-TRIB3 interaction attenuates NSCLC progression by accelerating EGFR degradation. |
| url |
https://doi.org/10.1038/s41467-020-17385-0 |
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