2c, d), CXCR7 knockdown may lead to an almost complete abrogation of in OT7 cells, in turn causing a significant downregulation of is finely regulated by the levels of SDF-1 and CXCR7 and, in turn, that CXCR4 regulates the expression of the ligand

2c, d), CXCR7 knockdown may lead to an almost complete abrogation of in OT7 cells, in turn causing a significant downregulation of is finely regulated by the levels of SDF-1 and CXCR7 and, in turn, that CXCR4 regulates the expression of the ligand. CXCR4 knockdown significantly reduced the proliferation of PD/S cells in both lineages, whereas CXCR7 knockdown only inhibited the proliferation of OT7 PD/S cells, in accordance with the strong downregulation of observed in these cells (Fig. invasion, promoting in vivo lung metastasis. Validation of these findings in patient samples of skin SCCs shows a strong correlation between the expression of and receptors in early WD-SCCs and advanced PD/S-SCCs of two different lineages of mouse skin SCC progression (OT7 and OT14). In each of these lineages, PD/S-SCCs were generated after the serial engraftment of their WD-SCC precursors in immunodeficient mice [11]. We found that expression, which was weakly detected in early SCCs, was upregulated in PD/S-SCCs (Fig. ?(Fig.1a).1a). In WD-SCCs, was expressed by fibroblasts (Fig. ?(Fig.1b)1b) and immunodetected in stromal cells (Fig. ?(Fig.1c),1c), as previously described [32, 35], whereas tumor cells and CD45+ immune cells (deficient in T-cell in nude immunodeficient mice) exhibited a faint or undetectable expression (Fig. ?(Fig.1b).1b). In contrast, SDF-1 was strongly upregulated in tumor cells of PD/S-SCCs (Fig. ?(Fig.1c),1c), reaching similar levels to those expressed by fibroblasts (Fig. ?(Fig.1b1b). Open in a separate window Fig. 1 CSCs of mouse advanced skin Dronedarone Hydrochloride SCCs express CXCR4 and CXCR7 and up-regulate the expression of mRNA relative to mRNA levels relative to in E-CSCs and L-CSCs (three different samples per group) isolated by FACS-sorter from the indicated tumors. h Flow cytometry quantification of CXCR4+ and CXCR7+ cells (red numbers) into the 6-integrin+/CD34+ Dronedarone Hydrochloride CSC population (blue numbers) of the indicated tumors. i Mean percentage (SE) of the indicated cell populations in WD-SCCs and PD/S-SCCs, as quantified in h. *, significant differences between compared groups (and expression was upregulated in advanced SCCs relative to WD-SCCs (Fig. ?(Fig.1d).1d). An expansion of CXCR4-expressing tumor cells was detected by immunohistochemistry in PD/S-SCCs, as compared to WD-SCCs (Supplementary Fig. 1A). Flow cytometry analysis showed that around 3C7% of tumor cells expressed CXCR4 (6-integrin+/CXCR4+ cells) in WD-SCCs, and this frequency was significantly increased in PD/S-SCCs (Fig. 1e, f). CXCR7+ cells were more frequent than CXCR4-expressing cells in early and advanced SCCs (Supplementary Fig. 1A and 1B). Accordingly, 60C70% of tumor cells expressed CXCR7 (6-integrin+/CXCR7+ cells) in WD-SCCs and this frequency was not significantly increased in PD/S-SCCs (Fig. 1e, f). Dronedarone Hydrochloride These results suggest that increased levels of mRNA detected in advanced tumors may be associated with a different stromal/tumor cells ratio in WD-SCCs and PD/S-SCCs [36, 37]. Analysis of the ligand and receptors in the CSC population (6-integrin+/CD34+ cells) showed that CSCs isolated from PD/S-SCCs (L-CSCs) strongly expressed and upregulation was observed in primary PD/S-SCCs (spontaneously developed in K14-HPV16 mice [11]) and in PD/S-SCCs that were engrafted in syngeneic immunocompetent mice, relative to their respective WD-SCCs (Supplementary Fig. 1C and 1D). SDF-1 expression was significantly induced in tumor and stromal cells (Supplementary Fig. 1E), and an expansion of CXCR4-expressing CSCs was detected in PD/S-SCCs generated in immunocompetent mice (Supplementary Fig. 1FC1H), indicating that SDF-1 signaling may be activated in CSCs of advanced tumors independently of the immune status of the mice. Autocrine SDF-1 signaling promotes PD/S-SCC CSC proliferation and invasion To determine whether an autocrine SDF-1 signaling is induced in L-CSCs, we isolated tumor cells from WD-SCCs (WD cells) and PD/S-SCCs (PD/S cells), which were maintained Mouse monoclonal to ATXN1 in culture. We previously demonstrated that these primary cultures were enriched in tumor-initiating cells that conserved the molecular traits of parental SCC CSCs [11]. In this regard, PD/S cells expressed and secreted higher levels of SDF-1 than WD cells (Fig. 2a, b). In addition, PD/S cells expressed and than (Fig. ?(Fig.2c).2c). Accordingly, 40C60% of 6-integrin+/CD34+-CSCs in PD/S cell cultures expressed CXCR7, whereas 6C16% of 6-integrin+/CD34+-CSCs expressed CXCR4 (Fig. ?(Fig.2d;2d; Supplementary Fig. 2A and 2B), and most CXCR4+-CSCs expressed CXCR7 (Supplementary Fig. 2C). Open in a separate Dronedarone Hydrochloride window Fig. 2.