Disruption of Stat3 reveals a critical role in both the initiation and the promotion stages of epithelial carcinogenesis
J. Clin. Invest. Keith Syson Chan, et al. 114:720 doi:10.1172/JCI21032 [Go to this article.]

Figure 3
Response of Stat3-deficient keratinocytes to DMBA-induced apoptosis both in vitro and in vivo. (A and B) Cultures of primary keratinocytes from (A) control mice and (B) Stat3-deficient mice treated with DMBA. Scale bar: 200 μm. (C) Percentage of apoptotic cells in control (white bars) and Stat3-deficient (black bars) keratinocytes treated with DMBA. *P < 0.05 by Mann-Whitney U test. (D) Caspase-3 staining of epidermis from Stat3-deficient mice. Note that most of the caspase-3–positive cells are located in a restricted region of the hair follicles (arrows), while a smaller number are located in the interfollicular epidermis (arrowhead). IFE, interfollicular epidermis; HF, hair follicle; D, dermis. Scale bar: 100 μm. (E) Number of caspase-3–postive cells per centimeter of epidermis in control (white bars) and Stat3-deficient mice (black bars). *P < 0.05 and **P < 0.01 by Mann-Whitney U test. (F) Double staining of label-retaining cells (BrdU; red) and caspase-3–positive cells (green) in skin of Stat3-deficient mice treated with DMBA (25 nmol) and sacrificed 24 hours later. Scale bar: 20 μm. Dotted lines mark the margins of hair follicles, and “b” indicates the bulge region of hair follicle.