Obesity and cancer stem cells: Roles in cancer initiation, progression and therapy resistance

Table 1 Murine models of high-fat diet-induced obesity and cancer stem cells

Tissue	Findings	Ref.
Intestine	Increased crypt depth and villus height; increased number of Olmf4-positive ISCs; increased size of the enterospheres that developed from ISCs	[18]
Intestine	Increase in crypt depth; non-stem progenitor intestinal cells gain more stemness features and self-renewal; 50% increase in the number of Olfm4+ ISCs; 23% decrease in the number of Paneth cells; more likely to initiate mini-intestines; organoids had higher frequencies of Lgr5+ ISCs; ISCs by themselves had an increased capacity to initiate organoids	[19]
Intestine	Combined with Pten inactivation, obesity is insufficient to drive Lgr5+ ISC-derived tumorigenesis	[20]
Intestine	Increased aberrant crypt and crypt foci; increased proliferation of colonocytes per mouse	[21]
Intestine	Higher number of Lgr5+ stem cells per crypt	[22]
Intestine	Increased number of ISCs and progenitor cells; crypts are further likely to form mini-intestine organoids in a 3D culture	[23]
Intestine	Increased intestinal epithelial cell proliferation	[24]
Intestine	Reprograms Bmi1+ cells to function and persist as stem-like cells in mucosal homeostasis and tumor development	[25]
Intestine	Increased number of crypts; increased total numbers of ISCs and percentage of ISCs in S-phase; reduced numbers of Paneth and goblet cells	[26]
Lung	Increased number of AT2 cells; higher stem cell colony forming efficiency	[27]
Esophagus	Increased numbers of epithelial progenitors in Barrett’s esophagus	[28]

ISC: Intestinal stem cell; Lgr5: Leucine-rich repeat-containing G protein-coupled receptor 5; AT2: Alveolar type-2.