Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc
Abstract Actin filament associated protein 1 antisense RNA 1 (named AFAP1-AS1) is a long non-coding RNA and overexpressed in many cancers. This study aimed to identify the role and mechanism of AFAP1-AS1 in lung cancer. The AFAP1-AS1 expression was firstly assessed in 187 paraffin-embedded lung canc...
| Main Authors: | , , , , , , , , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Nature Publishing Group
2021-06-01
|
| Series: | Signal Transduction and Targeted Therapy |
| Online Access: | https://doi.org/10.1038/s41392-021-00562-y |
| _version_ | 1818928234519068672 |
|---|---|
| author | Yu Zhong Liting Yang Fang Xiong Yi He Yanyan Tang Lei Shi Songqing Fan Zheng Li Shanshan Zhang Zhaojian Gong Can Guo Qianjin Liao Yujuan Zhou Ming Zhou Bo Xiang Xiaoling Li Yong Li Zhaoyang Zeng Guiyuan Li Wei Xiong |
| author_facet | Yu Zhong Liting Yang Fang Xiong Yi He Yanyan Tang Lei Shi Songqing Fan Zheng Li Shanshan Zhang Zhaojian Gong Can Guo Qianjin Liao Yujuan Zhou Ming Zhou Bo Xiang Xiaoling Li Yong Li Zhaoyang Zeng Guiyuan Li Wei Xiong |
| author_sort | Yu Zhong |
| collection | DOAJ |
| description | Abstract Actin filament associated protein 1 antisense RNA 1 (named AFAP1-AS1) is a long non-coding RNA and overexpressed in many cancers. This study aimed to identify the role and mechanism of AFAP1-AS1 in lung cancer. The AFAP1-AS1 expression was firstly assessed in 187 paraffin-embedded lung cancer and 36 normal lung epithelial tissues by in situ hybridization. The migration and invasion abilities of AFAP1-AS1 were investigated in lung cancer cells. To uncover the molecular mechanism about AFAP1-AS1 function in lung cancer, we screened proteins that interact with AFAP1-AS1 by RNA pull down and the mass spectrometry analyses. AFAP1-AS1 was highly expressed in lung cancer clinical tissues and its expression was positively correlated with lung cancer patients’ poor prognosis. In vivo experiments confirmed that AFAP1-AS1 could promote lung cancer metastasis. AFAP1-AS1 promoted lung cancer cells migration and invasion through interacting with Smad nuclear interacting protein 1 (named SNIP1), which inhibited ubiquitination and degradation of c-Myc protein. Upregulation of c-Myc molecule in turn promoted the expression of ZEB1, ZEB2, and SNAIL gene, which ultimately enhanced epithelial to mesenchymal transition (EMT) and lung cancer metastasis. Understanding the molecular mechanism by which AFAP1-AS1 promotes lung cancer’s migration and invasion may provide novel therapeutic targets for lung cancer patients’ early diagnosis and therapy. |
| first_indexed | 2024-12-20T03:25:40Z |
| format | Article |
| id | doaj.art-920d0bf417c84ecf81f322cb5c439495 |
| institution | Directory Open Access Journal |
| issn | 2059-3635 |
| language | English |
| last_indexed | 2024-12-20T03:25:40Z |
| publishDate | 2021-06-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Signal Transduction and Targeted Therapy |
| spelling | doaj.art-920d0bf417c84ecf81f322cb5c4394952022-12-21T19:55:06ZengNature Publishing GroupSignal Transduction and Targeted Therapy2059-36352021-06-016111310.1038/s41392-021-00562-yLong non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-MycYu Zhong0Liting Yang1Fang Xiong2Yi He3Yanyan Tang4Lei Shi5Songqing Fan6Zheng Li7Shanshan Zhang8Zhaojian Gong9Can Guo10Qianjin Liao11Yujuan Zhou12Ming Zhou13Bo Xiang14Xiaoling Li15Yong Li16Zhaoyang Zeng17Guiyuan Li18Wei Xiong19NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Science, Central South UniversityDepartment of Neurosurgery, Xiangya Hospital, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityDepartment of Oral and Maxillofacial Surgery, the Second Xiangya Hospital, Central South UniversityDepartment of Oral and Maxillofacial Surgery, the Second Xiangya Hospital, Central South UniversityKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Science, Central South UniversityDepartment of Neurosurgery, Xiangya Hospital, Central South UniversityDepartment of Oral and Maxillofacial Surgery, the Second Xiangya Hospital, Central South UniversityKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Science, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityDepartment of Medicine, Dan L Duncan Comprehensive Cancer Center, Baylor College of MedicineNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital, Xiangya School of Medicine, Central South UniversityAbstract Actin filament associated protein 1 antisense RNA 1 (named AFAP1-AS1) is a long non-coding RNA and overexpressed in many cancers. This study aimed to identify the role and mechanism of AFAP1-AS1 in lung cancer. The AFAP1-AS1 expression was firstly assessed in 187 paraffin-embedded lung cancer and 36 normal lung epithelial tissues by in situ hybridization. The migration and invasion abilities of AFAP1-AS1 were investigated in lung cancer cells. To uncover the molecular mechanism about AFAP1-AS1 function in lung cancer, we screened proteins that interact with AFAP1-AS1 by RNA pull down and the mass spectrometry analyses. AFAP1-AS1 was highly expressed in lung cancer clinical tissues and its expression was positively correlated with lung cancer patients’ poor prognosis. In vivo experiments confirmed that AFAP1-AS1 could promote lung cancer metastasis. AFAP1-AS1 promoted lung cancer cells migration and invasion through interacting with Smad nuclear interacting protein 1 (named SNIP1), which inhibited ubiquitination and degradation of c-Myc protein. Upregulation of c-Myc molecule in turn promoted the expression of ZEB1, ZEB2, and SNAIL gene, which ultimately enhanced epithelial to mesenchymal transition (EMT) and lung cancer metastasis. Understanding the molecular mechanism by which AFAP1-AS1 promotes lung cancer’s migration and invasion may provide novel therapeutic targets for lung cancer patients’ early diagnosis and therapy.https://doi.org/10.1038/s41392-021-00562-y |
| spellingShingle | Yu Zhong Liting Yang Fang Xiong Yi He Yanyan Tang Lei Shi Songqing Fan Zheng Li Shanshan Zhang Zhaojian Gong Can Guo Qianjin Liao Yujuan Zhou Ming Zhou Bo Xiang Xiaoling Li Yong Li Zhaoyang Zeng Guiyuan Li Wei Xiong Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc Signal Transduction and Targeted Therapy |
| title | Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc |
| title_full | Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc |
| title_fullStr | Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc |
| title_full_unstemmed | Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc |
| title_short | Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc |
| title_sort | long non coding rna afap1 as1 accelerates lung cancer cells migration and invasion by interacting with snip1 to upregulate c myc |
| url | https://doi.org/10.1038/s41392-021-00562-y |
| work_keys_str_mv | AT yuzhong longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT litingyang longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT fangxiong longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT yihe longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT yanyantang longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT leishi longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT songqingfan longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT zhengli longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT shanshanzhang longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT zhaojiangong longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT canguo longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT qianjinliao longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT yujuanzhou longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT mingzhou longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT boxiang longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT xiaolingli longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT yongli longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT zhaoyangzeng longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT guiyuanli longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc AT weixiong longnoncodingrnaafap1as1accelerateslungcancercellsmigrationandinvasionbyinteractingwithsnip1toupregulatecmyc |