RECK expression in cervicitis, CIN I, CIN II/III and invasive cervical carcinomas.

<p>n = 66;</p>*<p>Weak = no staining or faint staining;</p>**<p>Strong = moderate or strong staining.</p

Expression of HPV-16 E6/E7 down-regulates RECK in organotypic cultures.

<p><i>A,</i> Representative immunoreactivity of RECK in control and HPV16 E6E7 expressing rafts cultures. Note the strong RECK membrane staining pattern (black arrow) in control compared to the faint staining in HPV16 E6E7 expressing rafts cultures. <i>B,</i> Quantitative real-time PCR (qRT-PCR) of <i>RECK</i> expression in organotypic cultures. The relative expression levels were normalized to tubulin. Bars represent the means of triplicate experiments; <i>bars</i>, ±SE.</p

HPV16 oncoproteins down-regulate RECK and TIMP-2 in HFKs.

<p><i>A,</i> Monolayer cultures of primary HFKs were transduced with pLXSN-based retroviral vectors expressing HPV16 E6wt and/or E7wt. RECK levels were determined by Western blot. Beta-actin was used as loading control. FF287 cell line was used as a positive control. <i>B,</i> Immunofluorescence detection of RECK (<i>green</i>) in HFKs expressing HPV oncoproteins. RECK is clearly detected in control and HPV16 E6wt expressing HFKs, while E7wt and E6E7-expressing cells exhibit reduced protein levels (<i>arrows</i>). Nuclei were counterstained with DAPI (<i>blue</i>). Original magnification 1000×. <i>C,</i> TIMP-2 was determined by ELISA (Biotrak). <i>P<0.05</i>.</p

RECK is down-regulated in CIN II/III and invasive carcinoma samples.

<p>Representative immunoreactivity of RECK in (A) Cervicitis, (B) cervical intraepithelial neoplasia II (CIN II), (C) cervical intraepithelial neoplasia III (CIN III) and (D) cervical invasive carcinoma. Note the strong RECK membrane staining pattern in cervicitis (black arrow), a diminished cytoplasmastic staining in CIN II/III and a very weak RECK staining in invasive carcinoma. Inset in (D): Sample incubated in the absence of primary antibody.</p