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Figure 9 | Molecular Cancer

Figure 9

From: DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells

Figure 9

Proposed working models for the postulated crosstalk among DTX3L, ARTD8 and ARTD9 in chemotherapy-resistant mPCa cells. (A) Constitutively active IL6/STAT3-signaling and enhanced IFNGR-JAK1/2-STAT1- signaling in chemotherapy-resistant mPCa cells, including CRPC-like cells causes overexpression of DTX3L and ARTD9, which in turn, further stimulates their own expression through a positive feedback loop. (B) Crosstalk between DTX3L/ARTD9-STAT1 and ARTD8-STAT6-signaling pathways is required for proliferation and cell survival of chemotherapy-resistant mPCa cells, including CRPC-like cells. (C) Similar to the situation in HR-DLBCL, DTX3L and ARTD9, together with STAT1β repress the transcriptional activation of the tumor suppressor IRF1 and other anti-proliferative and pro-apoptotic genes while together with STAT1α both, DTX3L and ARTD9 might activate genes required for cell proliferation and survival of mPCa cells. (D) Overexpression of DTX3L but not ARTD8 or ARTD9 also mediates cell migration of mPCa cells, dependent on STAT1 and STAT3-signaling. DTX3L might form migration-specific, ARTD9-independent STAT1 homodimer or non-canonical STAT1/STAT3 heterodimer complexes.

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Molecular Cancer

ISSN: 1476-4598