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- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2018.1
- 수록면
- 1,009 - 1,022 (14page)
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Purpose Glioblastoma (GBM) is classified as one of the most aggressive and lethal brain tumor. Great strides have been made in understanding the genomic and molecular underpinnings of GBM, which translated into development of new therapeutic approaches to combat such deadly disease. However, there are only few therapeutic agents that can effectively inhibit GBM invasion in a clinical framework. In an effort to address such challenges, we have generated anti-SEMA3A monoclonal antibody as a potential therapeutic antibody against GBM progression. Materials and Methods We employed public glioma datasets, Repository of Molecular Brain Neoplasia Data and The Cancer Genome Atlas, to analyze SEMA3AmRNA expression in human GBM specimens. We also evaluated for protein expression level of SEMA3A via tissue microarray (TMA) analysis. Cell migration and proliferation kinetics were assessed in various GBM patient-derived cells (PDCs) and U87-MG cell-line for SEMA3A antibody efficacy. GBM patient-derived xenograft (PDX) models were generated to evaluate tumor inhibitory effect of anti-SEMA3A antibody in vivo. Results By combining bioinformatics and TMA analysis, we discovered that SEMA3A is highly expressed in human GBM specimens compared to non-neoplastic tissues. We developed three different anti-SEMA3A antibodies, in fully human IgG form, through screening phagedisplayed synthetic antibody library using a classical panning method. Neutralization of SEMA3A significantly reduced migration and proliferation capabilities of PDCs and U87-MG cell line in vitro. In PDX models, treatment with anti-SEMA3A antibody exhibited notable tumor inhibitory effect through down-regulation of cellular proliferative kinetics and tumorassociated macrophages recruitment. Conclusion In present study, we demonstrated tumor inhibitory effect of SEMA3A antibody in GBM progression and present its potential relevance as a therapeutic agent in a clinical framework.
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참고문헌 (29)
참고문헌 신청
Adamson C / 2009 / Glioblastoma multiforme: a review of where we have been and where we are going / Expert Opin Investig Drugs 18:1061~1083
Louis DN / 2007 / The 2007 WHO classification of tumours of the central nervous system / Acta Neuropathol 114:97~109
Reardon DA / 2006 / Therapeutic advances in the treatment of glioblastoma: rationale and potential role of targeted agents / Oncologist 11:152~164
Stupp R / 2005 / Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma / N Engl J Med 352:987~996
Linger RM / 2008 / TAM receptor tyrosine kinases: biologic functions, signaling, and potential therapeutic targeting in human cancer / Adv Cancer Res 100:35~83
Louis DN / 2007 / The 2007 WHO classification of tumours of the central nervous system / Acta Neuropathol 114:97~109
Reardon DA / 2006 / Therapeutic advances in the treatment of glioblastoma: rationale and potential role of targeted agents / Oncologist 11:152~164
Stupp R / 2005 / Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma / N Engl J Med 352:987~996
Linger RM / 2008 / TAM receptor tyrosine kinases: biologic functions, signaling, and potential therapeutic targeting in human cancer / Adv Cancer Res 100:35~83
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