Fig. 8From: HDAC2 depletion promotes osteosarcoma’s stemness both in vitro and in vivo: a study on a putative new target for CSCs directed therapyProposed mechanistic model of HDAC2 function in osteosarcoma. Decrease of HDAC2 or DNMT3a expression or loss of both inhibits the formation of HDAC2/DNMT3a complex leading to transcription of genes involved in osteosarcomas stemness and promoting tumor initiation and progressionBack to article page