摘要
原文 | 英語 |
---|---|
頁(從 - 到) | 756-771 |
頁數 | 16 |
期刊 | Molecular Oncology |
卷 | 12 |
發行號 | 5 |
DOIs | |
出版狀態 | 已發佈 - 五月 1 2018 |
指紋
ASJC Scopus subject areas
- Molecular Medicine
- Genetics
- Cancer Research
引用此文
Serum amyloid A1 in combination with integrin αVβ3 increases glioblastoma cells mobility and progression. / Lin, Ching Yu; Yang, Shun Tai; Shen, Shing Chuan; Hsieh, Yi Chen; Hsu, Fei Ting; Chen, Cheng Yu; Chiang, Yung Hsiao; Chuang, Jian Ying; Chen, Kai Yun; Hsu, Tsung I.; Leong, Wan Chong; Su, Yu Kai; Lo, Wei Lun; Yeh, Yi Shian; Patria, Yudha Nur; Shih, Hsiu Ming; Chang, Che Chang; Chou, Szu Yi.
於: Molecular Oncology, 卷 12, 編號 5, 01.05.2018, p. 756-771.研究成果: 雜誌貢獻 › 文章
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TY - JOUR
T1 - Serum amyloid A1 in combination with integrin αVβ3 increases glioblastoma cells mobility and progression
AU - Lin, Ching Yu
AU - Yang, Shun Tai
AU - Shen, Shing Chuan
AU - Hsieh, Yi Chen
AU - Hsu, Fei Ting
AU - Chen, Cheng Yu
AU - Chiang, Yung Hsiao
AU - Chuang, Jian Ying
AU - Chen, Kai Yun
AU - Hsu, Tsung I.
AU - Leong, Wan Chong
AU - Su, Yu Kai
AU - Lo, Wei Lun
AU - Yeh, Yi Shian
AU - Patria, Yudha Nur
AU - Shih, Hsiu Ming
AU - Chang, Che Chang
AU - Chou, Szu Yi
PY - 2018/5/1
Y1 - 2018/5/1
N2 - Glioblastoma multiforme (GBM) is a highly malignant type of brain tumor found in humans. GBM cells reproduce quickly, and the median survival time for patients after therapy is approximately 1 year with a high relapse rate. Current therapies and diagnostic tools for GBM are limited; therefore, we searched for a more favorable therapeutic target or marker protein for both therapy and diagnosis. We used mass spectrometry (MS) analysis to identify GBM-associated marker proteins from human plasma and GBM cell cultures. Additional plasma and 52 brain tissues obtained from patients with gliomas were used to validate the association rate of serum amyloid A1 (SAA1) in different grades of gliomas and its distribution in tumors. Microarray database analysis further validated the coefficient of SAA1 levels in gliomas. The cellular mechanisms of SAA1 in GBM proliferation and infiltration were investigated in vitro. We analyzed the correlation between SAA1 and patients' medication requirement to demonstrate the clinical effects of SAA1 in GBM. SAA1 was identified from MS analysis, and its level was revealed to be correlated with the disease grade, clinical severity, and survival rate of patients with gliomas. In vitro cultures, including GBM cells and normal astrocytes, revealed that SAA1 promotes cell migration and invasion through integrin αVβ3 to activate the Erk signaling pathway. Magnetic resonance imaging and tumor region-specific microarray analysis identified a correlation between SAA1 and GBM cell infiltration in patients. In summary, our results demonstrate that SAA1 in combination with integrin αV and β3 can serve as an indicator of high glioblastoma risk. We also identified the cellular mechanisms of SAA1 contributing to GBM progression, which can serve as the basis for future GBM therapy.
AB - Glioblastoma multiforme (GBM) is a highly malignant type of brain tumor found in humans. GBM cells reproduce quickly, and the median survival time for patients after therapy is approximately 1 year with a high relapse rate. Current therapies and diagnostic tools for GBM are limited; therefore, we searched for a more favorable therapeutic target or marker protein for both therapy and diagnosis. We used mass spectrometry (MS) analysis to identify GBM-associated marker proteins from human plasma and GBM cell cultures. Additional plasma and 52 brain tissues obtained from patients with gliomas were used to validate the association rate of serum amyloid A1 (SAA1) in different grades of gliomas and its distribution in tumors. Microarray database analysis further validated the coefficient of SAA1 levels in gliomas. The cellular mechanisms of SAA1 in GBM proliferation and infiltration were investigated in vitro. We analyzed the correlation between SAA1 and patients' medication requirement to demonstrate the clinical effects of SAA1 in GBM. SAA1 was identified from MS analysis, and its level was revealed to be correlated with the disease grade, clinical severity, and survival rate of patients with gliomas. In vitro cultures, including GBM cells and normal astrocytes, revealed that SAA1 promotes cell migration and invasion through integrin αVβ3 to activate the Erk signaling pathway. Magnetic resonance imaging and tumor region-specific microarray analysis identified a correlation between SAA1 and GBM cell infiltration in patients. In summary, our results demonstrate that SAA1 in combination with integrin αV and β3 can serve as an indicator of high glioblastoma risk. We also identified the cellular mechanisms of SAA1 contributing to GBM progression, which can serve as the basis for future GBM therapy.
KW - glioblastoma multiform
KW - integrin αVβ3
KW - invasion
KW - metastasis
KW - serum amyloid A1
UR - http://www.scopus.com/inward/record.url?scp=85045848628&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85045848628&partnerID=8YFLogxK
U2 - 10.1002/1878-0261.12196
DO - 10.1002/1878-0261.12196
M3 - Article
C2 - 29603594
AN - SCOPUS:85045848628
VL - 12
SP - 756
EP - 771
JO - Molecular Oncology
JF - Molecular Oncology
SN - 1574-7891
IS - 5
ER -