scholarly journals The prognostic value of polycomb group protein B-cell-specific moloney murine leukemia virus insertion site 1 in stage II colon cancer patients

Apmis ◽  
2016 ◽  
Vol 124 (7) ◽  
pp. 541-546 ◽  
Author(s):  
Maiken L. M. Espersen ◽  
Dorte Linnemann ◽  
Ib J. Christensen ◽  
Mahdi Alamili ◽  
Jesper T. Troelsen ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Prognostic Value ◽  
Leukemia Virus ◽  
Insertion Site ◽  
Polycomb Group ◽  
Moloney Murine Leukemia Virus ◽  
Polycomb Group Protein ◽  
Group Protein ◽  
Stage Ii Colon Cancer ◽  
Murine Leukemia

Provirus Insertion Site of Moloney Murine Leukemia Virus 1 Pim-1

2012 ◽  
pp. 1488-1488
Author(s):  
Dominique M. Donato ◽  
Steven K. Hanks ◽  
Kenneth A. Jacobson ◽  
M. P. Suresh Jayasekara ◽  
Zhan-Guo Gao ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Insertion Site ◽  
Moloney Murine Leukemia Virus ◽  
Murine Leukemia

Structural Basis of Inhibitor Specificity of the Human Protooncogene Proviral Insertion Site in Moloney Murine Leukemia Virus (PIM-1) Kinase

2005 ◽  
Vol 48 (24) ◽  
pp. 7604-7614 ◽  
Author(s):  
Alex N. Bullock ◽  
Judit É. Debreczeni ◽  
Oleg Y. Fedorov ◽  
Adam Nelson ◽  
Brian D. Marsden ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Insertion Site ◽  
Moloney Murine Leukemia Virus ◽  
Structural Basis ◽  
Inhibitor Specificity ◽  
Murine Leukemia

scholarly journals Doublecortin-Like Kinase 1 (DCLK1) Regulates B Cell-Specific Moloney Murine Leukemia Virus Insertion Site 1 (Bmi-1) and is Associated with Metastasis and Prognosis in Pancreatic Cancer

2018 ◽  
Vol 51 (1) ◽  
pp. 262-277 ◽  
Author(s):  
Jian Li ◽  
Yunchao Wang ◽  
Jiayun Ge ◽  
Wenhua Li ◽  
Liangyu Yin ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
B Cell ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Insertion Site ◽  
Moloney Murine Leukemia Virus ◽  
Murine Leukemia

Background/Aims: Cancer stem cells (CSCs) are largely responsible for tumor relapse and metastatic behavior. Doublecortin-like kinase 1 (DCLK1) was recently reported to be a biomarker for gastrointestinal CSCs and involved in the epithelial-mesenchymal transition (EMT) and tumor progression. B cell-specific Moloney murine leukemia virus insertion site 1 (Bmi-1) is a crucial regulator of CSC self-renewal, malignant transformation and EMT, and a previous study from our group showed that Bmi-1 is upregulated in pancreatic cancer progression and participates in EMT. However, it remains unclear whether DCLK1 is involved in pancreatic cancer or whether DCLK1 is associated with the altered level of Bmi-1 expression. Methods: The correlation of DCLK1 expression and clinical features of pancreatic cancer was analyzed in 210 paraffin-embedded archived pancreatic cancer specimens by immunohistochemical analysis. The biological effects of DCLK1 siRNA on cells were investigated by examining cell proliferation using a cell counting kit and cell colony assays, cell migration by wound healing assay and cell invasion by Transwell invasion assay. We further investigated the effect of therapeutic siRNA targeting DCLK1 on pancreatic cancer cell growth in vivo. Moreover, the molecular mechanism by which DCLK1 upregulates Bmi-1 expression was explored using real-time PCR, western blotting and Co-immunoprecipitation assay. Results: DCLK1 is overexpressed in pancreatic cancer and is related to metastasis and prognosis. Knockdown of DCLK1 markedly suppressed cell growth in vitro and in vivo and also inhibited the migration and invasion of pancreatic cancer cells. Furthermore, we found that DCLK1 silencing could inhibit EMT in cancer cells via downregulation of Bmi-1 and the mesenchymal markers Snail and Vimentin and upregulation of the epithelial marker E-cadherin. Moreover, high DCLK1 expression in human pancreatic cancer samples was associated with a mesenchymal phenotype and increased cell proliferation. Further co-immunoprecipitation indicated that DCLK1 did not interact with Bmi-1 directly. Conclusion: Our data suggest that upregulation of DCLK1 may contribute to pancreatic cancer metastasis and poor prognosis by increasing Bmi-1 expression indirectly. The findings indicate that inhibiting DCLK1 expression might be a novel strategy for pancreatic cancer therapy.

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