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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.1
- 수록면
- 198 - 202 (5page)
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초록· 키워드
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Comprehensive inhibition of RUNX1, RUNX2, and RUNX3 led to marked cell suppression compared with inhibition of RUNX1 alone, clarifying that the RUNX family members are important for proliferation and maintenance of diverse cancers, and “cluster regulation of RUNX (CROX)” is a very effective strategy to suppress cancer cells. Recent studies reported by us and other groups suggested that wild-type RUNX1 is needed for survival and proliferation of certain types of leukemia, lung cancer, gastric cancer, etc. and for their one of metastatic target sites such as born marrow endothelial niche, suggesting that RUNX1 often functions oncogenic manners in cancer cells. In this review, we describe the significance and paradoxical requirement of RUNX1 tumor suppressor in leukemia and even solid cancers based on recent our findings such as “genetic compensation of RUNX family transcription factors (the compensation mechanism for the total level of RUNX family protein expression)”, “RUNX1 inhibition-induced inhibitory effects on leukemia cells and on solid cancers through p53 activation”, and “autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells”. Taken together, these findings identify a crucial role for the RUNX cluster in the maintenance and progression of cancers and suggest that modulation of the RUNX cluster using the pyrrole-imidazole polyamide gene-switch technology is a potential novel therapeutic approach to control cancers.
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참고문헌 (22)
참고문헌 신청
Bando, T. / 2006 / Synthesis and biological properties of sequence-specific DNA-alkylating pyrrole-imidazole polyamides / Acc. Chem. Res 39:935~944
Best, T. P. / 2003 / Nuclear localization of pyrrole-imidazole polyamide-fluorescein conjugates in cell culture / Proc. Natl. Acad. Sci. U. S. A 100:12063~12068
Goyama, S. / 2013 / Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells / J. Clin. Invest 123:3876~3888
Hyde, R. K. / 2010 / Cbfb/Runx1 repression-independent blockage of differentiation and accumulation of Csf2rb-expressing cells by Cbfb-MYH11 / Blood 115:1433~1443
Hyde, R. K. / 2015 / Runx1 is required for hematopoietic defects and leukemogenesis in Cbfb-MYH11 knock-in mice / Leukemia 29:1771~1778
Best, T. P. / 2003 / Nuclear localization of pyrrole-imidazole polyamide-fluorescein conjugates in cell culture / Proc. Natl. Acad. Sci. U. S. A 100:12063~12068
Goyama, S. / 2013 / Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells / J. Clin. Invest 123:3876~3888
Hyde, R. K. / 2010 / Cbfb/Runx1 repression-independent blockage of differentiation and accumulation of Csf2rb-expressing cells by Cbfb-MYH11 / Blood 115:1433~1443
Hyde, R. K. / 2015 / Runx1 is required for hematopoietic defects and leukemogenesis in Cbfb-MYH11 knock-in mice / Leukemia 29:1771~1778
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The Clinical, Molecular, and Mechanistic Basis of RUNX1 Mutations Identified in Hematological Malignancies
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Identification a novel de novo RUNX2 frameshift mutation associated with cleidocranial dysplasia
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Tour d’Horizon of Recent Advances in RUNX Family Gene Research
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Involvement of RUNX and BRD Family Members in Restriction Point
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Human umbilical cord mesenchymal stem cells overexpressing RUNX1 promote tendon-bone healing by inhibiting osteolysis, enhancing osteogenesis and promoting angiogenesis
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Complex Interplay between the RUNX Transcription Factors and Wnt/β-Catenin Pathway in Cancer: A Tango in the Night
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The RUNX1 Enhancer Element eR1: A Versatile Marker for Adult Stem Cells
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K-Ras?Activated Cells Can Develop into Lung Tumors When Runx3-Mediated Tumor Suppressor Pathways Are Abrogated
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RUNX1 Mutations in the Leukemic Progression of Severe Congenital Neutropenia
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RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down Syndrome
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RUNX1 Ameliorates Rheumatoid Arthritis Progression through Epigenetic Inhibition of LRRC15
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Hypoxia Mediates Runt-Related Transcription Factor 2 Expression via Induction of Vascular Endothelial Growth Factor in Periodontal Ligament Stem Cells
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