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Sci. STKE, 30 January 2007
Vol. 2007, Issue 371, p. pe4
[DOI: 10.1126/stke.3712007pe4]


EGFR Signaling Inhibits E2F1-Induced Apoptosis in Vivo: Implications for Cancer Therapy

Doron Ginsberg*

Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan 52900, Israel.

Abstract: The retinoblastoma tumor suppressor (RB) restricts cell proliferation by regulating members of the E2F family of transcription factors. In human tumors RB is often inactivated, resulting in aberrant E2F-dependent transcription and uncontrolled proliferation. One of the E2F proteins, E2F1, can also induce apoptosis. The extent of E2F1-induced apoptosis is known to be tissue- and cell-specific, but until now, it has been unclear what variables determine cellular sensitivity to E2F1-induced apoptosis in vivo. A recent study reveals epidermal growth factor receptor (EGFR) signaling to be one such variable, as EGFR signaling cooperates with RB in inhibiting E2F1-induced apoptosis. This finding raises the possibility that therapeutic manipulation of EGFR signaling may specifically trigger the death of cancer cells with inactive RB, thereby enabling "targeted" cancer treatments.

*Corresponding author. E-mail, ginsbed{at}

Citation: D. Ginsberg, EGFR Signaling Inhibits E2F1-Induced Apoptosis in Vivo: Implications for Cancer Therapy. Sci. STKE 2007, pe4 (2007).

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