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PDZ-binding kinase aggravates pancreatic neuroendocrine neoplasm progression by activating the AKT/mTOR pathway.
Feng, Tingting; Jiang, Ruibin; Yin, Lu; Xu, Chenyang; Ma, Jian; Yin, Wenjuan; Jin, Jiaoyue; Lu, Tingting; Liu, Xinyuan; Lyu, Yingqi; Yang, Ying; Ying, Lisha; Hu, Qichao; Su, Dan; Ling, Sunbin.
Afiliação
  • Feng T; Department of Pathology, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
  • Jiang R; Cancer Research Institute, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
  • Yin L; Department of Hepatobiliary and Pancreatic Surgery, The Center for Integrated Oncology and Precision Medicine, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
  • Xu C; Department of Oncology, The First Clinical Medical College of Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • Ma J; Department of Immunology, Harbin Medical University, Harbin, Heilongjiang, China.
  • Yin W; Department of Pathology, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
  • Jin J; Department of Pathology, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
  • Lu T; Department of Oncology, The First Clinical Medical College of Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • Liu X; The Second Clinical Medical College, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
  • Lyu Y; Department of Oncology, The First Clinical Medical College of Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • Yang Y; The Second Clinical Medical College, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
  • Ying L; Cancer Research Institute, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
  • Hu Q; Key Laboratory of Digital Technology in Medical Diagnostics of Zhejiang Province, Dian Diagnostics Group Co. Ltd., Hangzhou, Zhejiang, China.
  • Su D; Department of Pathology, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
  • Ling S; Department of Hepatobiliary and Pancreatic Surgery, The Center for Integrated Oncology and Precision Medicine, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Mol Carcinog ; 62(5): 716-726, 2023 05.
Article em En | MEDLINE | ID: mdl-36807309
ABSTRACT
The therapeutic effects of existing drug regimens against pancreatic neuroendocrine neoplasms (pNENs) remain limited, and identifying ideal therapeutic targets is warranted. PDZ binding kinase (PBK) may play an oncogenic role in most solid tumors. However, its function in pNEN remains unclear. In this study, pNEN samples and International Cancer Genome Consortium data were used to determine the clinical significance of PBK. Cell counting and CCK8 assays were used to assess cell proliferation. Flow cytometry was used to assess drug-induced apoptosis and cell cycle arrest. An in vivo PBK-targeting experiment was performed in mice bearing pNENs. Western blotting, quantitative PCR, and immunohistochemistry were performed to assess the molecular mechanisms. PBK was significantly upregulated in pNEN tissues compared with paracancerous tissues. Additionally, PBK was a poor prognostic factor for pNEN patients. PBK was found to promote the proliferation of pNEN cells by activating the AKT/mTOR pathway. Furthermore, PBK inhibition combined with everolimus treatment had enhanced antitumour effects on pNEN via inhibiting AKT/mTOR pathway and inducing G0/G1 phase cell cycle arrest. This study highlights that PBK plays an oncogenic role in and is a promising therapeutic target for pNEN.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Pancreáticas / Tumores Neuroendócrinos / Quinases de Proteína Quinase Ativadas por Mitógeno Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Mol Carcinog Assunto da revista: BIOLOGIA MOLECULAR / NEOPLASIAS Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Pancreáticas / Tumores Neuroendócrinos / Quinases de Proteína Quinase Ativadas por Mitógeno Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Mol Carcinog Assunto da revista: BIOLOGIA MOLECULAR / NEOPLASIAS Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China