Abstract：
:The degree of heterogeneity among cancer stem cells (CSC) remains ill-defined and may hinder effective anti-CSC therapy. Evaluation of oral cancers for such heterogeneity identified two compartments within the CSC pool. One compartment was detected using a reporter for expression of the H3K4me3 demethylase JARID1B to isolate a JARID1B(high) fraction of cells with stem cell-like function. JARID1B(high) cells expressed oral CSC markers including CD44 and ALDH1 and showed increased PI3K pathway activation. They were distinguished from a fraction in a G0-like cell-cycle state characterized by low reactive oxygen species and suppressed PI3K/AKT signaling. G0-like cells lacked conventional CSC markers but were primed to acquire stem cell-like function by upregulating JARID1B, which directly mediated transition to a state expressing known oral CSC markers. The transition was regulated by PI3K signals acting upstream of JARID1B expression, resulting in PI3K inhibition depleting JARID1B(high) cells but expanding the G0-like subset. These findings define a novel developmental relationship between two cell phenotypes that may jointly contribute to CSC maintenance. Expansion of the G0-like subset during targeted depletion of JARID1B(high) cells implicates it as a candidate therapeutic target within the oral CSC pool. Cancer Res; 76(18); 5538-49. ©2016 AACR.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Facompre ND,Harmeyer KM,Sole X,Kabraji S,Belden Z,Sahu V,Whelan K,Tanaka K,Weinstein GS,Montone KT,Roesch A,Gimotty PA,Herlyn M,Rustgi AK,Nakagawa H,Ramaswamy S,Basu Ddoi
10.1158/0008-5472.CAN-15-3377subject
Has Abstractpub_date
2016-09-15 00:00:00pages
5538-49issue
18eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-15-3377journal_volume
76pub_type
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