EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc
The EI24 autophagy-associated transmembrane protein is frequently associated with tumor growth and patient survival. In the present study, we found that EI24 was downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues compared with adjacent normal tissues and was associated with cancer cell...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Gastroenterology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2018/2626545 |
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| author | Yi Zang Lei Zhu Tong Li Qi Wang Juanjuan Li Yuting Qian Lumin Wei Mingping Xie Wen-Hao Tang Xu Liu Ying Zhu Lifu Wang |
| author_facet | Yi Zang Lei Zhu Tong Li Qi Wang Juanjuan Li Yuting Qian Lumin Wei Mingping Xie Wen-Hao Tang Xu Liu Ying Zhu Lifu Wang |
| author_sort | Yi Zang |
| collection | DOAJ |
| description | The EI24 autophagy-associated transmembrane protein is frequently associated with tumor growth and patient survival. In the present study, we found that EI24 was downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues compared with adjacent normal tissues and was associated with cancer cell differentiation. Overexpression of EI24 suppressed cancer cell growth in vitro and in vivo and induced cell cycle S phase arrest, with no impact on caspase-dependent apoptosis. EI24 overexpression also resulted in reduced c-Myc expression, an oncogene in PDAC, accompanied with increased LC3B-II formation, increased Beclin-1, and diminished p62. Together, we propose that EI24 suppresses cell proliferation and prompts cell cycle arrest in pancreatic cancer cells by activating the autophagic lysosomal degradation of c-Myc. Our results suggest a potential mechanism underlying the antitumor effects of EI24 in PDAC and provide insight into the crosstalk between autophagy and cell proliferation involving a possible EI24/Beclin-1/p62/c-Myc signaling pathway. |
| format | Article |
| id | doaj-art-0d2175974d8242f7bb9cc09deac68cac |
| institution | Kabale University |
| issn | 1687-6121 1687-630X |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Gastroenterology Research and Practice |
| spelling | doaj-art-0d2175974d8242f7bb9cc09deac68cac2025-02-03T01:20:03ZengWileyGastroenterology Research and Practice1687-61211687-630X2018-01-01201810.1155/2018/26265452626545EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-MycYi Zang0Lei Zhu1Tong Li2Qi Wang3Juanjuan Li4Yuting Qian5Lumin Wei6Mingping Xie7Wen-Hao Tang8Xu Liu9Ying Zhu10Lifu Wang11Department of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of General Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of General Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaDepartment of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, ChinaThe EI24 autophagy-associated transmembrane protein is frequently associated with tumor growth and patient survival. In the present study, we found that EI24 was downregulated in pancreatic ductal adenocarcinoma (PDAC) tissues compared with adjacent normal tissues and was associated with cancer cell differentiation. Overexpression of EI24 suppressed cancer cell growth in vitro and in vivo and induced cell cycle S phase arrest, with no impact on caspase-dependent apoptosis. EI24 overexpression also resulted in reduced c-Myc expression, an oncogene in PDAC, accompanied with increased LC3B-II formation, increased Beclin-1, and diminished p62. Together, we propose that EI24 suppresses cell proliferation and prompts cell cycle arrest in pancreatic cancer cells by activating the autophagic lysosomal degradation of c-Myc. Our results suggest a potential mechanism underlying the antitumor effects of EI24 in PDAC and provide insight into the crosstalk between autophagy and cell proliferation involving a possible EI24/Beclin-1/p62/c-Myc signaling pathway.http://dx.doi.org/10.1155/2018/2626545 |
| spellingShingle | Yi Zang Lei Zhu Tong Li Qi Wang Juanjuan Li Yuting Qian Lumin Wei Mingping Xie Wen-Hao Tang Xu Liu Ying Zhu Lifu Wang EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc Gastroenterology Research and Practice |
| title | EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc |
| title_full | EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc |
| title_fullStr | EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc |
| title_full_unstemmed | EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc |
| title_short | EI24 Suppresses Tumorigenesis in Pancreatic Cancer via Regulating c-Myc |
| title_sort | ei24 suppresses tumorigenesis in pancreatic cancer via regulating c myc |
| url | http://dx.doi.org/10.1155/2018/2626545 |
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