Expression of the cell cycle regulator p27Kip1 in normal squamous epithelium, cervical intraepithelial neoplasia, and invasive squamous cell carcinoma of the uterine cervix

Shiozawa, Tanri; Shiohara, Shigeki; Kanai, Masashi; Konishi, Ikuo; Fujii, Shingo; Nikaido, Toshio

doi:10.1002/1097-0142(20011215)92:12<3005::aid-cncr10153>3.0.co;2-6

Cited by 24 publications

(34 citation statements)

References 70 publications

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“…Expressions of the cell-cycle-related molecules in cultured normal glandular cells after estrogen treatment were examined by Western blotting as described previously (Shiozawa et al, 2001b).…”

Section: Western Blottingmentioning

confidence: 99%

“…Complex formation between cyclin D1 and cdk4, as well as cyclin E and cdk2, in E2-treated (10 À6 M, 24 h) and E2-untreated normal endometrial glandular cells was examined by immunoprecipitation as previously described (Shiozawa et al, 2001b). The detection of associated proteins was carried out using antibodies against cyclin D1 (Progen, Heidelberg, Germany) and cyclin E (Santa Cruz Biotechnology).…”

Section: Immunoprecipitationmentioning

confidence: 99%

“…The kinase activity of the cyclin D1/cdk4 and cyclin E/cdk2 complexes in E2-treated (10 À6 M, 24 h) and E2-untreated normal endometrial glandular cells was evaluated by the detection of radio-labeled histone H1 protein as previously described (Shiozawa et al, 2001b).…”

Section: Histone H1 Kinase Assaymentioning

confidence: 99%

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Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence

et al. 2004

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To explore the mechanism of estrogen-induced growth of normal endometrium, the transactivation system of the cyclin D1 gene was analysed using cultured normal endometrial glandular cells. Estradiol (E2) treatment of cultured normal endometrial glandular cells induced upregulation of c-Jun, and then cyclin D1 proteins, followed by serial expressions of cyclins E, A and B1 proteins. Increase in the mRNA expression of cyclin D1 preceded the protein expression of cyclin D1 under E2 treatment. A luciferase assay using deletion constructs of the cyclin D1 promoter indicated that E2-induced increase in transcriptional activity was observed in reporters containing AP-1-binding site sequence, and that in the absence of E2, cotransfection of c-Jun also showed increase of transcriptional activity in the same reporters with AP-1 sequence. A gel shift assay using nuclear extract from E2-treated endometrial glandular cells and AP-1 sequences of the cyclin D1 promoter indicated specific binding between c-Jun protein and the promoter. Transfection of c-jun antisense oligonucleotides to the glandular cells resulted in the suppression of the E2-induced upregulation of cyclin D1 mRNA and protein. These findings suggest that E2-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of cJun to the AP-1 sequences.

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Section: Western Blottingmentioning

confidence: 99%

Section: Immunoprecipitationmentioning

confidence: 99%

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Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence

et al. 2004

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“…Interestingly, high levels of p27 have been shown to be a marker of poor prognosis in HPV-positive cervical cancers (Dellas et al, 1998;Shiozawa et al, 2001). The activity of the serine/threonine kinase Akt, a known modulator of p27 localization (Shin et al, 2002), is also increased in HPV-positive cervical lesions when compared to normal surrounding tissue and in E7-expressing human foreskin keratinocytes (HFKs) differentiated in organotypic raft culture (Menges et al, 2006).…”

mentioning

confidence: 99%

The E7 protein from human papillomavirus type 16 enhances keratinocyte migration in an Akt-dependent manner

Charette

McCance

2007

Oncogene

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“…In uterine cervical carcinomas, we have recently found that elevated expression of p27 was associated with increased growth activities, and our in vitro studies suggested the insufficient function of p27 in malignant tumors [43]. Paradoxical overexpression of p27 in human malignancies is an interesting issue which needs further clarification.…”

Section: Discussionmentioning

confidence: 83%

Inverse correlation between Skp2 and p27^Kip1in normal endometrium and endometrial carcinoma

Miyamoto

Horiuchi

Kashima

et al. 2010

Gynecological Endocrinology

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Cyclin-dependent-kinase (cdk) inhibitor, p27 Kip1 (p27), has been shown to participate in progestin-induced growth suppression of normal endometrial glands. To analyze the molecular mechanisms regulating p27 protein, we examined immunohistochemical expression of the SCF Skp2 complex factors, i.e., Skp1, Cul1 and Skp2, and compared them with that of p27, steroid receptors and Ki-67. In normal endometrial glands, the expression of Skp2 was observed in the proliferative phase, whereas that of p27 was observed in the secretory phase. Cultured normal endometrial glandular cells showed that progesterone induced the down-regulation of Skp2 along with up-regulation of p27. In endometrial carcinomas, the inverse topological correlation between Skp2 and p27 was evident in 39/66 (59%) cases, and the expression of Skp2 showed a strong correlation with Ki-67. These findings suggest that the expression of SCF Skp2 complex changes during the menstrual cycle in normal endometrium and the SCF Skp2 ubiquitin-proteasome pathway may also work in endometrial carcinomas.

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Expression of the cell cycle regulator p27Kip1 in normal squamous epithelium, cervical intraepithelial neoplasia, and invasive squamous cell carcinoma of the uterine cervix

Cited by 24 publications

References 70 publications

Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence

Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence

The E7 protein from human papillomavirus type 16 enhances keratinocyte migration in an Akt-dependent manner

Inverse correlation between Skp2 and p27^Kip1in normal endometrium and endometrial carcinoma

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Expression of the cell cycle regulator p27Kip1 in normal squamous epithelium, cervical intraepithelial neoplasia, and invasive squamous cell carcinoma of the uterine cervix

Cited by 24 publications

References 70 publications

Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence

Estrogen-induced proliferation of normal endometrial glandular cells is initiated by transcriptional activation of cyclin D1 via binding of c-Jun to an AP-1 sequence

The E7 protein from human papillomavirus type 16 enhances keratinocyte migration in an Akt-dependent manner

Inverse correlation between Skp2 and p27Kip1in normal endometrium and endometrial carcinoma

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Inverse correlation between Skp2 and p27^Kip1in normal endometrium and endometrial carcinoma