Musaad Alfayez1, Radhakrishnan Vishnubalaji2, Nehad M Alajez2. 1. Stem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia alfayez@ksu.edu.sa. 2. Stem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Abstract
BACKGROUND/AIM: Altered expression of runt-related transcription factor 1 (RUNX1T1) has been observed in several human cancer types; however, the exact role for RUNX1T1 in colorectal cancer (CRC) remains unclear. MATERIALS AND METHODS: The GSE21510 CRC and our previously published datasets were utilized in this study. Gene-expression profiling was conducted using the Agilent microarray platform, while data normalization and bioinformatics were conducted using GeneSpring software. AlamarBlue assay was used to assess cell viability in vitro. RESULTS: The expression of RUNX1T1 was severely down-regulated in primary CRC and cell lines. Lentiviral-mediated re-expression of RUNX1T1 inhibited CRC cell growth, and global gene-expression analysis revealed the cell cycle, DNA replication, and DNA damage as the pathways most affected by RUNX1T1. Forced expression of RUNX1T1 induced a significant reduction in cellular proliferation and sensitized CRC cells to 5-flurouracil. CONCLUSION: Our data revealed a novel role for RUNX1T1 as a tumor-suppressor gene in CRC through modulation of multiple cellular pathways. Copyright
BACKGROUND/AIM: Altered expression of runt-related transcription factor 1 (RUNX1T1) has been observed in several humancancer types; however, the exact role for RUNX1T1 in colorectal cancer (CRC) remains unclear. MATERIALS AND METHODS: The GSE21510 CRC and our previously published datasets were utilized in this study. Gene-expression profiling was conducted using the Agilent microarray platform, while data normalization and bioinformatics were conducted using GeneSpring software. AlamarBlue assay was used to assess cell viability in vitro. RESULTS: The expression of RUNX1T1 was severely down-regulated in primary CRC and cell lines. Lentiviral-mediated re-expression of RUNX1T1 inhibited CRC cell growth, and global gene-expression analysis revealed the cell cycle, DNA replication, and DNA damage as the pathways most affected by RUNX1T1. Forced expression of RUNX1T1 induced a significant reduction in cellular proliferation and sensitized CRC cells to 5-flurouracil. CONCLUSION: Our data revealed a novel role for RUNX1T1 as a tumor-suppressor gene in CRC through modulation of multiple cellular pathways. Copyright
Authors: Michael F Z Wang; Madhav Mantri; Shao-Pei Chou; Gaetano J Scuderi; David W McKellar; Jonathan T Butcher; Charles G Danko; Iwijn De Vlaminck Journal: Nat Commun Date: 2021-04-12 Impact factor: 14.919