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Cooperation between Constitutive and Inducible Chemokines Enables T-cell Engraftment and Immune Attack in Solid Tumors

ABSTRACT: Cooperation between Constitutive and Inducible Chemokines Enables T-cell Engraftment and Immune Attack in Solid Tumors

PROVIDER: PRJNA540658 | ENA |

REPOSITORIES: ENA

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Cooperation between Constitutive and Inducible Chemokines Enables T-cell Engraftment and Immune Attack in Solid Tumors

Project description:We investigated the role of chemokines in regulating T-cell accumulation in solid tumors. CCL5 and CXCL9 overexpression was associated with CD8+ T-cell infiltration in common solid tumors. T-cell infiltration required tumor cell-derived CCL5 and was amplified by IFN-dependent, myeloid cell-secreted CXCL9. Accordingly, CCL5-CXCL9 co-expression revealed immunoreactive tumors with prolonged survival and response to checkpoint blockade. Loss of CCL5 expression in human tumors was associated with epigenetic silencing through DNA methylation. Reduction of CCL5 expression caused TIL desertification whereas forced CCL5 expression prevented Cxcl9 and TIL loss and attenuated tumor growth in mice through IFN. The cooperation between tumor-derived CCL5 and IFN-inducible CXCR3 ligands secreted by myeloid cells is key for orchestrating T-cell infiltration in immunoreactive and immunoresponsive tumors.

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Cooperation between Constitutive and Inducible Chemokines Enables T Cell Engraftment and Immune Attack in Solid Tumors.

Project description:We investigated the role of chemokines in regulating T cell accumulation in solid tumors. CCL5 and CXCL9 overexpression was associated with CD8+ T cell infiltration in solid tumors. T cell infiltration required tumor cell-derived CCL5 and was amplified by IFN-?-inducible, myeloid cell-secreted CXCL9. CCL5 and CXCL9 coexpression revealed immunoreactive tumors with prolonged survival and response to checkpoint blockade. Loss of CCL5 expression in human tumors was associated with epigenetic silencing through DNA methylation. Reduction of CCL5 expression caused tumor-infiltrating lymphocyte (TIL) desertification, whereas forced CCL5 expression prevented Cxcl9 expression and TILs loss, and attenuated tumor growth in mice through IFN-?. The cooperation between tumor-derived CCL5 and IFN-?-inducible CXCR3 ligands secreted by myeloid cells is key for orchestrating T cell infiltration in immunoreactive and immunoresponsive tumors.

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Project description:Increased expression of chemokines in UNC1999-treated tumor tissues were successfully checked out through chemokines profiles screening of a total 25 different mouse chemokines using control and UNC1999-treated tumor tissues.

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Translation cooperation of FGF and WNT signaling

Project description:Cooperation between FGF and WNT signaling is well documented in normal development, stem cell biology and cancer progression. However, the molecular mechanisms underlying this cooperativity remain poorly understood. In this study, we employed an inducible FGFR1 to interrogate the dynamics of RNA, ribosome occupancy and protein expression as a function of FGFR signaling in the mouse mammary gland with constitutive WNT hyperactivation. We demonstrate that FGFR signaling increases the translation efficiency of WNT signaling components with structured 5’ UTRs harboring a (CGG)4 motif that can potentially form G-quadruplex structures, and that tumorigenesis driven by this mechanism is vulnerable to inhibition of eIF4A, a RNA helicase important in translation initiation. This study also provides novel insights into the contribution of RNA levels and translational regulation to protein expression in pre-malignant mammary epithelial cells dynamically responding to FGFR signaling.

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