A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages (original) (raw)

“…Although it is difficult to determine which event occurs first, a likely explanation is that EMT contributes to the establishment of CSCs. EMT has been described to upregulate the expression of CD90 on breast cancer and lung cancer cells [38,40]. Furthermore, EMT has been demonstrated to occur in pNETs, since positive immunohistochemical staining of human INS and INS of Rip1tag2 mice was found for SNAI1 and TWIST [11].…”

Section: Discussionmentioning

“…Furthermore, the engagement of membrane-type M-CSF expressed on cancer cells with CD115 on macrophages contributes to this cell-cell interaction (16). Moreover, TAMs support tumorigenic activities and trigger resistance to anticancer drugs by inducing cancer-stem cell properties in tumor cells (28)(29)(30). However, we did not observe myeloid cell-mediated induction of TIM-3 on RCC cell lines in vitro, although RCC tumors express TIM-3 in the vicinity of macrophages in clinical samples.…”

Section: Discussionmentioning

“…Indeed, TAMs can sustain CSC proliferation by releasing proinflammatory cytokines such as TNF-α and IL-6, which reinforce tumor cell proliferation through NF-κB and STAT3 signaling pathways (96,97). These same molecular pathways may be activated through a direct TAM-to-CSC contact via CD90 and ephrin A4 receptors (98). Finally, the crosstalk between CSCs and TAMs induced TAM secretion of milk fat globule EGF factor 8 (MFGE8) and IL-6, which favored CSC reservoir survival during chemotherapeutic treatment (99).…”

Section: Mdsc-and Tam-dependent Protumoral Aidmentioning