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Currently, there are three methods for enriching osteosarcoma CSCs: (1) generating sarcospheres in culture, (2) cell sorting with markers (CD133, ALDH, CD117 combined with Stro-1), and (3) exogenously expressing human Oct4 promoter [5].
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GSIs were shown to reduce glioblastoma CSCs [70] and breast CSCs [71] through inhibition of Notch pathway.
IL-6 activated JAK2/STAT3 pathway was proposed to support the maintenance of CD24-CD44+ CD24-CD44+s [85].
This was demonstrated by Al-Hajj et al. when describing tumor-initiating breast CSCs [8].
miR-200c inhibited the polycomb gene Bmi-1 in breast CSCs, leading to reduced self-renewal of CSCs [109].
Madjd et al. also showed that BCL-2 was highly expressed in CD44+/CD24-/low CD44+/CD24-/low].
Inhibition of NF-κB by Eriocalyxin B induced cell death in chemoresistant CD44+ ovarian CSCs [90].
A recent study showed that transcription factor Oct1 directly regulates ABC transporter genes Abcg2, Abcb1 and Abcb4 in CSCs [38].
The extent of Wnt activation was positively correlated with expression of well-studied cell surface makers for CSCs [63].
Hotair is also highly expressed in CD133+CD44+ colon cancer cells which have been characterized as EMT CSCs [120].
The miR-181 family which interacts with the TGF-β pathway functions in the regulation of EMT breast CSCs [113].
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