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dc.contributor.author
Hu, Weiwei
dc.contributor.author
Zheng, Shufang
dc.contributor.author
Guo, Haixin
dc.contributor.author
Dai, Beiying
dc.contributor.author
Ni, Jiaping
dc.contributor.author
Shi, Yaohong
dc.contributor.author
Bian, Hanrui
dc.contributor.author
Li, Lanxin
dc.contributor.author
Shen, Yumeng
dc.contributor.author
Wu, Mo
dc.contributor.author
Tian, Zhoutong
dc.contributor.author
Liu, Guilai
dc.contributor.author
Hossain, Md Amir
dc.contributor.author
Yang, Hongbao
dc.contributor.author
Wang, Duowei
dc.contributor.author
Zhang, Qin
dc.contributor.author
Yu, Jun
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Feng, Jifeng
dc.contributor.author
Yu, Decai
dc.contributor.author
Yang, Yong
dc.date.available
2022-10-04T12:56:47Z
dc.date.issued
2021-02
dc.identifier.citation
Hu, Weiwei; Zheng, Shufang; Guo, Haixin; Dai, Beiying; Ni, Jiaping; et al.; PLAGL2-EGFR-HIF-1/2α Signaling Loop Promotes HCC Progression and Erlotinib Insensitivity; John Wiley & Sons Inc.; Hepatology (Baltimore, Md.); 73; 2; 2-2021; 674-691
dc.identifier.issn
0270-9139
dc.identifier.uri
http://hdl.handle.net/11336/171666
dc.description.abstract
Background and Aims: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, hence a major public health threat. Pleomorphic adenoma gene like-2 (PLAGL2) has been reported to play a role in tumorigenesis. However, its precise function in HCC remains poorly understood. Approach and Results: In this study, we demonstrated that PLAGL2 was up-regulated in HCC compared with that of adjacent nontumorous tissues and also correlated with overall survival times. We further showed that PLAGL2 promoted HCC cell proliferation, migration, and invasion both in vitro and in vivo. PLAGL2 expression was positively correlated with epidermal growth factor receptor (EGFR) expression. Mechanistically, this study demonstrated that PLAGL2 functions as a transcriptional regulator of EGFR and promotes HCC cell proliferation, migration, and invasion through the EGFR-AKT pathway. Moreover, hypoxia was found to significantly induce high expression of PLAGL2, which promoted hypoxia inducible factor 1/2 alpha subunit (HIF1/2A) expression through EGFR. Therefore, this study demonstrated that a PLAGL2-EGFR-HIF1/2A signaling loop promotes HCC progression. More importantly, PLAGL2 expression reduced hepatoma cells’ response to the anti-EGFR drug erlotinib. PLAGL2 knockdown enhanced the response to erlotinib. Conclusions: This study reveals the pivotal role of PLAGL2 in HCC cell proliferation, metastasis, and erlotinib insensitivity. This suggests that PLAGL2 can be a potential therapeutic target of HCC.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
John Wiley & Sons Inc.
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dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
PLAGL2-EGFR-HIF1/2A
dc.subject.classification
Biología Celular, Microbiología
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
PLAGL2-EGFR-HIF-1/2α Signaling Loop Promotes HCC Progression and Erlotinib Insensitivity
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2022-09-09T17:22:19Z
dc.journal.volume
73
dc.journal.number
2
dc.journal.pagination
674-691
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
New Jersey
dc.description.fil
Fil: Hu, Weiwei. China Pharmaceutical University; China
dc.description.fil
Fil: Zheng, Shufang. China Pharmaceutical University; China
dc.description.fil
Fil: Guo, Haixin. China Pharmaceutical University; China
dc.description.fil
Fil: Dai, Beiying. China Pharmaceutical University; China
dc.description.fil
Fil: Ni, Jiaping. China Pharmaceutical University; China
dc.description.fil
Fil: Shi, Yaohong. China Pharmaceutical University; China
dc.description.fil
Fil: Bian, Hanrui. China Pharmaceutical University; China
dc.description.fil
Fil: Li, Lanxin. China Pharmaceutical University; China
dc.description.fil
Fil: Shen, Yumeng. China Pharmaceutical University; China
dc.description.fil
Fil: Wu, Mo. China Pharmaceutical University; China
dc.description.fil
Fil: Tian, Zhoutong. China Pharmaceutical University; China
dc.description.fil
Fil: Liu, Guilai. China Pharmaceutical University; China
dc.description.fil
Fil: Hossain, Md Amir. China Pharmaceutical University; China
dc.description.fil
Fil: Yang, Hongbao. China Pharmaceutical University; China
dc.description.fil
Fil: Wang, Duowei. China Pharmaceutical University; China
dc.description.fil
Fil: Zhang, Qin. Jiangsu Cancer Hospital; China
dc.description.fil
Fil: Yu, Jun. Jiangsu Cancer Hospital; China
dc.description.fil
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
dc.description.fil
Fil: Feng, Jifeng. Jiangsu Cancer Hospital; China
dc.description.fil
Fil: Yu, Decai. Medical School Of Nanjing University; China
dc.description.fil
Fil: Yang, Yong. China Pharmaceutical University; China
dc.journal.title
Hepatology (Baltimore, Md.)
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1002/hep.31293
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep.31293
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