Research Paper Volume 9, Issue 1 pp 114—132

Induction of fibroblast senescence generates a non-fibrogenic myofibroblast phenotype that differentially impacts on cancer prognosis

Figure 1. Senescent CAF analyzed ex vivo and in vivo are predominantly SMA-positive. (A) Histogram showing percentage of cells positive for senescence-associated (SA)-β-Galactosidase or SMA-positive stress fiber formation in normal oral fibroblasts (POF) and cancer-associated oral fibroblasts (CAF) grown ex-vivo. Data are presented as Mean ±SEM from 6 POFs and 6 CAF. (B) Representative images of immunohistochemistry on sequential tissue sections of SMA-positive/p16-positive or SMA-positive/p16-negative HNSCC cases. (C) Pie chart showing the percentage of HNSCC cases with stromal staining for SMA or p16. (D) Representative image of double immunofluorescence staining of a p16-positive/SMA-positive HNSCC case showing co-expression of SMA (red) and p16 (green, white arrows; scale bars represent 25µm). (E) Representative immunohistochemistry for SMA and markers of senescence (p53, p21) and oxidative stress (8-OHDG) on sequential tissue sections of HNSCC. See also Supplementary Fig. S2.