KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling
SNIP1 methylation initiates its oncogenic functions. Here, the authors show that SNIP1 is methylated by KMT5A and this leads to downstream signalling that activates the YAP pathway, resulting in tumorigenesis and metastasis.
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2022-04-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-022-29899-w |
| _version_ | 1828349139295928320 |
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| author | Bo Yu Jun Su Qiqi Shi Qing Liu Jun Ma Guoqing Ru Lei Zhang Jian Zhang Xichun Hu Jianming Tang |
| author_facet | Bo Yu Jun Su Qiqi Shi Qing Liu Jun Ma Guoqing Ru Lei Zhang Jian Zhang Xichun Hu Jianming Tang |
| author_sort | Bo Yu |
| collection | DOAJ |
| description | SNIP1 methylation initiates its oncogenic functions. Here, the authors show that SNIP1 is methylated by KMT5A and this leads to downstream signalling that activates the YAP pathway, resulting in tumorigenesis and metastasis. |
| first_indexed | 2024-04-14T01:05:16Z |
| format | Article |
| id | doaj.art-400befdf8abf46fcacd2ea79a1f24e90 |
| institution | Directory Open Access Journal |
| issn | 2041-1723 |
| language | English |
| last_indexed | 2024-04-14T01:05:16Z |
| publishDate | 2022-04-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Nature Communications |
| spelling | doaj.art-400befdf8abf46fcacd2ea79a1f24e902022-12-22T02:21:15ZengNature PortfolioNature Communications2041-17232022-04-0113111810.1038/s41467-022-29899-wKMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signalingBo Yu0Jun Su1Qiqi Shi2Qing Liu3Jun Ma4Guoqing Ru5Lei Zhang6Jian Zhang7Xichun Hu8Jianming Tang9Department of Medical Oncology, Fudan University Shanghai Cancer CenterDepartment of Oncology, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of MedicineState Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, Shanghai Jiao Tong UniversityDepartment of Medical Oncology, Zhongshan Hospital, Fudan UniversityEye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan UniversityDepartment of Pathology, Zhejiang Provincial People’s Hospital, People’ s Hospital of Hangzhou Medical CollegeDepartment of Radiation Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong UniversityDepartment of Medical Oncology, Fudan University Shanghai Cancer CenterDepartment of Medical Oncology, Fudan University Shanghai Cancer CenterInstitute of Cancer Neuroscience, Medical Frontier Innovation Research Center, The First Hospital of Lanzhou University, The First Clinical Medical College of Lanzhou UniversitySNIP1 methylation initiates its oncogenic functions. Here, the authors show that SNIP1 is methylated by KMT5A and this leads to downstream signalling that activates the YAP pathway, resulting in tumorigenesis and metastasis.https://doi.org/10.1038/s41467-022-29899-w |
| spellingShingle | Bo Yu Jun Su Qiqi Shi Qing Liu Jun Ma Guoqing Ru Lei Zhang Jian Zhang Xichun Hu Jianming Tang KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling Nature Communications |
| title | KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling |
| title_full | KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling |
| title_fullStr | KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling |
| title_full_unstemmed | KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling |
| title_short | KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling |
| title_sort | kmt5a methylated snip1 promotes triple negative breast cancer metastasis by activating yap signaling |
| url | https://doi.org/10.1038/s41467-022-29899-w |
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