CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin
Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) in NPC. Down-regulation of was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic e...
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| Published in: | International journal of biological sciences Vol. 15; no. 9; pp. 1802 - 1815 |
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| Main Authors: | , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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| ISSN: | 1449-2288, 1449-2288 |
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| Abstract | Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG)
in NPC. Down-regulation of
was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers
could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis.
could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia.
could co-localize with adhesion molecule Integrin-β1, the expression of
was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that
could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion,
is a vital tumor suppressor in the carcinogenesis of NPC. |
|---|---|
| AbstractList | Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) CHL1 in NPC. Down-regulation of CHL1 was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers CHL1 could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis. CHL1 could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia. CHL1 could co-localize with adhesion molecule Integrin-β1, the expression of CHL1 was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that CHL1 could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion, CHL1 is a vital tumor suppressor in the carcinogenesis of NPC.Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) CHL1 in NPC. Down-regulation of CHL1 was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers CHL1 could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis. CHL1 could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia. CHL1 could co-localize with adhesion molecule Integrin-β1, the expression of CHL1 was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that CHL1 could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion, CHL1 is a vital tumor suppressor in the carcinogenesis of NPC. Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) CHL1 in NPC. Down-regulation of CHL1 was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers CHL1 could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis. CHL1 could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia. CHL1 could co-localize with adhesion molecule Integrin-β1, the expression of CHL1 was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that CHL1 could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion, CHL1 is a vital tumor suppressor in the carcinogenesis of NPC. Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) in NPC. Down-regulation of was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis. could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia. could co-localize with adhesion molecule Integrin-β1, the expression of was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion, is a vital tumor suppressor in the carcinogenesis of NPC. |
| Author | Kwong, Dora Lai-Wan Liu, Ming Zhu, Cai-Lei Tsao, Sai Wah Chen, Qian Liu, Wai Man Wang, Bo Chen, Jin-Na Chen, Chao Fu, Li Jiang, Chen Guan, Xin-Yuan Jiang, Ling-Xi Zhang, Li-Yi Tang, Hong Chen, Juan Xiang, Yan-Qun |
| AuthorAffiliation | 1 Departments of Clinical Oncology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China 6 Department of Nasopharyngeal, Sun Yat-Sen Cancer Center, Guangzhou, China 7 Guangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pharmacology and Shenzhen University International Cancer Research Centre, Shenzhen University school of Medicine, Shenzhen, China 3 Departments of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China 5 State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China 8 Department of Orthopedics, Union Hospital, Tongji Medical College, Science and Technology of Huazhong University, Wuhan, China 2 Department of Clinical Oncology, The Seventh Affiliated Hospital, Sun Yat-sen University 4 Departments of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China |
| AuthorAffiliation_xml | – name: 1 Departments of Clinical Oncology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China – name: 8 Department of Orthopedics, Union Hospital, Tongji Medical College, Science and Technology of Huazhong University, Wuhan, China – name: 4 Departments of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China – name: 7 Guangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pharmacology and Shenzhen University International Cancer Research Centre, Shenzhen University school of Medicine, Shenzhen, China – name: 2 Department of Clinical Oncology, The Seventh Affiliated Hospital, Sun Yat-sen University – name: 6 Department of Nasopharyngeal, Sun Yat-Sen Cancer Center, Guangzhou, China – name: 5 State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China – name: 3 Departments of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China |
| Author_xml | – sequence: 1 givenname: Juan surname: Chen fullname: Chen, Juan – sequence: 2 givenname: Chen surname: Jiang fullname: Jiang, Chen – sequence: 3 givenname: Li surname: Fu fullname: Fu, Li – sequence: 4 givenname: Cai-Lei surname: Zhu fullname: Zhu, Cai-Lei – sequence: 5 givenname: Yan-Qun surname: Xiang fullname: Xiang, Yan-Qun – sequence: 6 givenname: Ling-Xi surname: Jiang fullname: Jiang, Ling-Xi – sequence: 7 givenname: Qian surname: Chen fullname: Chen, Qian – sequence: 8 givenname: Wai Man surname: Liu fullname: Liu, Wai Man – sequence: 9 givenname: Jin-Na surname: Chen fullname: Chen, Jin-Na – sequence: 10 givenname: Li-Yi surname: Zhang fullname: Zhang, Li-Yi – sequence: 11 givenname: Ming surname: Liu fullname: Liu, Ming – sequence: 12 givenname: Chao surname: Chen fullname: Chen, Chao – sequence: 13 givenname: Hong surname: Tang fullname: Tang, Hong – sequence: 14 givenname: Bo surname: Wang fullname: Wang, Bo – sequence: 15 givenname: Sai Wah surname: Tsao fullname: Tsao, Sai Wah – sequence: 16 givenname: Dora Lai-Wan surname: Kwong fullname: Kwong, Dora Lai-Wan – sequence: 17 givenname: Xin-Yuan surname: Guan fullname: Guan, Xin-Yuan |
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| Keywords | nasopharyngeal carcinoma tumor metastasis tumor suppressor gene tumor invasion |
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| References | 36778119 - Int J Biol Sci. 2023 Jan 5;19(3):829-830 |
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| Snippet | Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3... |
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| SubjectTerms | 1-Phosphatidylinositol 3-kinase AKT protein Antibodies Biopsy Blotting, Western Carcinogenesis Carcinogens Cdc42 protein Cell Adhesion Molecules - genetics Cell Adhesion Molecules - metabolism Cell cycle Cell Cycle Checkpoints - genetics Cell Cycle Checkpoints - physiology Cell growth Cell Line Cell Movement - genetics Cell Movement - physiology CHL1 protein Chromosome 3 Chromosome deletion Chromosomes Clonal deletion Committees Deactivation DNA Methylation - genetics DNA Methylation - physiology Ectopic expression Esophagus Filopodia Fluorescent Antibody Technique Gene expression Genes Human subjects Humans Immunoprecipitation Inactivation Integrin beta1 - metabolism Lamellipodia Lung cancer Markers Mesenchyme Metastases Metastasis Nasopharyngeal carcinoma Nasopharyngeal Carcinoma - genetics Nasopharyngeal Carcinoma - metabolism Neurofibromin 2 - metabolism Pathogenesis Promoter Regions, Genetic - genetics Proto-Oncogene Proteins c-akt - metabolism Rac1 protein Real-Time Polymerase Chain Reaction Research Paper RhoA protein RNA Interference Signal transduction Signal Transduction - genetics Signal Transduction - physiology Signaling Survival Tumor suppressor genes Tumors |
| Title | CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin |
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