Interactome analysis reveals molecular mechanisms underlying the association between selenium binding protein 1 expression and the malignant features of tumor cells
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- Tajima Takashi
- Division of Rare Cancer Research, National Cancer Center Research Institute
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- Kito Fusako
- Division of Rare Cancer Research, National Cancer Center Research Institute
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- Ohta Tsutomu
- Division of Rare Cancer Research, National Cancer Center Research Institute
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- Shiozawa Kumiko
- Division of Rare Cancer Research, National Cancer Center Research Institute
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- Kawai Akira
- Division of Musculoskeletal Oncology, National Cancer Center Hospital
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- Kondo Tadashi
- Division of Rare Cancer Research, National Cancer Center Research Institute
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抄録
The potential biological and clinical significance of selenium binding protein 1 (SBP1) has been suggested in various types of cancer. To evaluate the role of SBP1 and reveal the molecular basis for its function, we examined the SBP1 protein complex. A gene transfection assay revealed that overexpression of SBP1 promoted proliferation and migration of A549 lung adenocarcinoma cells. Halo-tag-based affinity purification coupled with liquid chromatography-tandem mass spectrometry identified 23 components of the SBP1 protein complex. The functional classification of these 23 proteins suggests that the SBP1 complex participates in critical biological events including cell structure, protein translation, stress response, chaperone, and apoptosis. Moreover, the SBP1 complex includes several proteins that are aberrantly expressed in cancers. These finding indicate that SBP1 may function coordinately with these multiple proteins to facilitate cancer progression. A comprehensive study of the multiple proteins associated with SPB1 together with an examination of individual proteins will be required to elucidate the roles of aberrant SBP1 regulation in cancer progression.
収録刊行物
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- Journal of Electrophoresis
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Journal of Electrophoresis 59 (1), 1-6, 2015
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詳細情報 詳細情報について
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- CRID
- 1390001205228595456
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- NII論文ID
- 130005130417
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- ISSN
- 13499408
- 13499394
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可