Sasa quelpaertensis Leaf Extract Inhibits Colon Cancer by Regulating Cancer Cell Stemness in Vitro and in Vivo.

Abstract

A rare subpopulation of cancer cells, termed cancer stem cells (CSCs), may be responsible for tumor relapse and resistance to conventional chemotherapy. The development of a non-toxic, natural treatment for the elimination of CSCs is considered a strategy for cancer treatment with minimal side effects. In the present study, the potential for Sasa quelpaertensis leaf extract (SQE) and its two bioactive compounds, tricin and p-coumaric acid, to exert anti-CSC effects by suppressing cancer stemness characteristics were evaluated in colon cancer cells. CD133+CD44+ cells were isolated from HT29 and HCT116 cell lines using flow-activated cell sorting (FACs). SQE treatment was found to significantly suppress the self-renewal capacity of both cell lines. SQE treatment was also associated with the down-regulation of β-catenin and phosphorylated GSK3β, while significantly enhancing cell differentiation by up-regulating CK20 expression and blocking the expression of several stem cell markers, including DLK1, Notch1, and Sox-2. In vivo, SQE supplementation suppressed tumor growth in a xenograft model by down-regulating stem cell markers and β-catenin as well as HIF-1α signaling. Compared with two bioactive compounds of SQE, SQE exhibited the most effective anti-CSC properties. Taken together, these results provide evidence that SQE inhibits colon cancer by regulating the characteristics of CSCs.

• Authors: Soo Jin Min, Ji Ye Lim, Haeng Ran Kim, Se-Jae Kim, Yuri Kim
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 16 Issue 5 Pg. 9976-97 (Apr 30 2015) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 25941936 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• AC133 Antigen
• Antigens, CD
• Antineoplastic Agents
• Calcium-Binding Proteins
• DLK1 protein, human
• Glycoproteins
• Hyaluronan Receptors
• Hypoxia-Inducible Factor 1, alpha Subunit
• Intercellular Signaling Peptides and Proteins
• Membrane Proteins
• PROM1 protein, human
• Peptides
• Plant Extracts
• Prom1 protein, mouse
• Receptor, Notch1
• SOXB1 Transcription Factors
• beta Catenin
• GSK3B protein, human
• Glycogen Synthase Kinase 3 beta
• Gsk3b protein, mouse
• Glycogen Synthase Kinase 3

Topics

• AC133 Antigen
• Animals
• Antigens, CD (genetics, metabolism)
• Antineoplastic Agents (pharmacology, therapeutic use)
• Calcium-Binding Proteins
• Colonic Neoplasms (drug therapy)
• Female
• Glycogen Synthase Kinase 3 (genetics, metabolism)
• Glycogen Synthase Kinase 3 beta
• Glycoproteins (genetics, metabolism)
• HT29 Cells
• Humans
• Hyaluronan Receptors (genetics, metabolism)
• Hypoxia-Inducible Factor 1, alpha Subunit (metabolism)
• Intercellular Signaling Peptides and Proteins (genetics, metabolism)
• Membrane Proteins (genetics, metabolism)
• Mice
• Mice, Inbred BALB C
• Neoplastic Stem Cells (drug effects, metabolism)
• Peptides (genetics, metabolism)
• Plant Extracts (pharmacology, therapeutic use)
• Plant Leaves (chemistry)
• Receptor, Notch1 (genetics, metabolism)
• SOXB1 Transcription Factors (genetics, metabolism)
• Sasa (chemistry)
• beta Catenin (metabolism)