Skip to main content
Fig. 2 | BMC Cancer

Fig. 2

From: Nodal induces apoptosis and inhibits proliferation in ovarian endometriosis-clear cell carcinoma lesions

Fig. 2

Relationship of Nodal with pSmad2 in endometriosis-OCCCa/OEmCas. a Staining by hematoxylin and eosin (HE) and IHC for Nodal and pSmad2 in endometriosis, OCCCa, and OEmCa. Insets show the magnified views of the boxed areas. Original magnification, × 200, × 400 (inset). b IHC scores for Nodal and pSmad2 in endometriosis-OCCCa (left) and endometriosis-OEmCa (right). The data shown are means ± SDs. E1, endometriosis without carcinoma; E2, endometriosis with carcinoma; Ca, carcinoma. c Correlation between Nodal and pSmad2 scores in a combination of endometriosis and OCCCa (upper) or OEmCa (lower). d Left: staining by HE and ISH for TGF-β1 mRNA in endometriosis and OCCCa. Note the strong ISH signals in stromal components of endometriosis and OCCCa cells, in contrast to a lack of the signal in the epithelial element (indicated by arrow) in the former. Insets show the magnified views of the boxed areas. Original magnification, × 100 and × 400 (inset). Right: ISH scores for TGF-β1 in endometriosis (End) and OCCCa. e Left: RT-PCR (left upper) and western blot analyses (left lower) for the indicated molecules in Ishikawa cells following treatment with 0, 2, and 4 ng/mL TGF-β1 for 24 h. Right: Ishikawa cells were transfected with Nodal reporter constructs, together with cotransfection of Smad2 or treatment of 2 and 4 ng/mL TGF-β1 for 24 h. Relative activity was determined based on arbitrary light units of luciferase activity normalized to pRL-TK activity. The activities of the reporter plus the effector relative to that of the reporter plus empty vector are shown as means ± SDs. The experiment was performed in duplicate

Back to article page