The antitumor effects of interferon-alpha are maintained in mice challenged with a STAT1-deficient murine melanoma cell line

IFN-α-2b–Induced Signal Transduction and Gene Regulation in Patient Peripheral Blood Mononuclear Cells Is Not Enhanced by a Dose Increase from 5 to 10 Megaunits/m2

“…This prompted us to investigate if IFN-a was acting primarily as an immune activator. Using STAT1-deficient mice and STAT1-deficient melanoma tumor cells, our group showed that the antitumor effects of IFN-a are dependent on STAT1 signaling within immune cells and not the cancer cell (42,43). In lieu of a panel of ISGs that directly correlates with the antitumor effects of IFN-a, we have used the activation of JAK-STAT signaling intermediates as a marker of the ability of IFN-a to stimulate immune effector cells.…”

The Jak-STAT Signal Transduction Pathway in Melanoma

“…Since STAT1 deficient (STAT1 -/-) mice manifested deficiencies in IFN-mediated anti-viral immunity, we postulated that the anti-tumor effects of IFN-α might proceed primarily via immunologic mechanisms (Durbin, J. E. et al 1996). To explore the contribution of STAT1-mediated gene regulation within the tumor, our group generated a STAT1-deficient murine melanoma cell line, AGS-1 (Badgwell, B. et al 2004;. STAT1 was reconstituted within AGS-1 cells by retroviral gene transfer.…”

PTP1B and TC-PTP: regulators of transformation and tumorigenesis

“…STAT1-null mice are prone to develop solid tumors, and STAT1 has been described as a tumor suppressor in this system, acting downstream of type I and II interferons [105][106][107][108]. In particular, IFN-γ, a type II interferon, has been shown to be required for lymphocyte-mediated protection of tumor development [109].…”