Abstract
Abstract The cancer stem cells (CSCs) are thought to be responsible for recurrence and drug resistance after chemotherapy. CSCs markers are mostly studied in breast cancer and other cancers but study of CSCs marker is insufficient in GI cancers. LGR5 (Leucine-rich-repeat-containing G protein-coupled receptor5) is Wnt target gene that marks dividing stem cells such as hair follicle, intestine and stomach. Recently, the various evidences suggest LGR5 as cancer stem cell marker in colon cancer. However, its function and mechanism remain unclear. RUNX3(runt[[Unable to Display Character: ‑]]related transcription factor 3) is known as tumor suppressor gene in gastrointestinal epithelium. It is reported that loss of RUNX3 induces EMT, makes stem cell like subpopulation and reveals remarkable LGR5. But It is unclear whether upregulation of LGR5 influences tumorigenesis in colon CSC. Here we found that LGR5 is down-regulated when RUNX3 endogenously expressed whereas LGR5 is up-regulated when RUNX3 don't endogenously expressed in colon cancer. So, we confirm that overexpression of RUNX3 decrease proteinexpression of epithelial-mesenchymal transition(EMT) markers by western blotting and mRNA expression of LGR5, SOX2, OCT4, and NANOG by Real Time-PCR. We knockdown RUNX3 by siRNA in colon cancer cells that endogenously expressed RUNX3. The siRNA increases expression of LGR5. We performed colonosphere culture to measure size and number. Overexpression of RUNX3 decreases size, number and CSCs marker level whereas, knockdown of RUNX3 increases size, number and CSCs marker level in colonosphere formation. These studies suggest that role of Lgr5 as colon cancer stem cell marker and Runx3 known as tumor suppressor gene and aim to identify the mechanism of the metastasis of colon cancer and recurrence with Lgr5 and RUNX3. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):B54. Citation Format: Bo Ram Kim, Myoung Hee Kang, Jun Suk Kim, Sang Cheul Oh. Role and underlying mechanism of Runx3-Lgr5 in colon cancer cell lines. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr B54.
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