Targeting of the Bmi-1 oncogene/stem cell renewal factor by microRNA-128 inhibits glioma proliferation and self-renewal.

By J. Godlewski, M. Nowicki, Agnieszka Bronisz, Shante P. Williams, Akihiro Otsuki, G. Nuovo, A. Raychaudhury, H. Newton, E. Chiocca, S. Lawler. Cancer Research, 2008

744 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/16d0ef38edb45acb164c7ce772924f04e4c5003b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Thomas Brabletz
2. Danish H Sayed
3. Simone Brabletz
4. Marc P. Stemmler
5. M. Abdellatif
6. M. Nieto

In Molecular Biology

1. Thomas Brabletz
2. Simone Brabletz
3. Marc P. Stemmler
4. Danish H Sayed
5. Y. Lee
6. O. Schmalhofer
7. M. Abdellatif
8. R. Weinberg

Citations in the corpus

• The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs (2009, result): “Transient overexpression of these miRNAs had no effect on levels of Bmi1 mRNA, in contrast to miR-128, recently found to be a regulator of Bmi1 (ref”
• Reprogramming of miRNA networks in cancer and leukemia. (2010, neutral): “…E-TABM-42 (Calin et al. 2005), E-TABM-48 (Roldo et al. 2006), E-TABM-22 (Yanaihara et al. 2006), E-TABM-23 (Iorio et al. 2005), E- TABM-46, E-TABM-47, E-TABM-49, and E-TABM-50 (Volinia et al. 2006), and E-MEXP-1796 (Godlewski et al. 2008), E-TABM-37 (Ciafre et al. 2005), E-TABM-341 (Ueda et al.).”
• Cancer Stem Cells (CSCs) in Drug Resistance and their Therapeutic Implications in Cancer Treatment (2018, background): “The usage of miRNA as CSC-based therapeutic agents is reported; for example, mir-22 that targets TET2 in leukemia (AML and MDS) and breast cancer [194], Let-7 to target RAS and HMGA2 in breast cancer [195], mir-128 to target BMI-1 in brain cancer [191], mir-200 to target ZEB1/ZEB2, BMI-1, and SUZ12 ”
• MicroRNAs in development and disease. (2011, background): “Moreover, downregulation of miR-128 enhances the expression of its target Bmi-1 (208), which suppresses PTEN and increases AKT activity (570).”