title: Up-regulation of pS2 expression during the development of adenocarcinomas but not squamous cell carcinomas of the uterine cervix, independently of expression of c-jun or oestrogen and progesterone receptors.
abstract: The pS2 gene product was firstly identified as an oestrogen-induced molecule in a breast cancer cell line, while recent studies demonstrate a close association with mucus-secreting epithelia. To assess pS2 expression in uterine cervical adenocarcinomas (C-ACas) and invasive squamous cell carcinomas (C-ISCCs), a series of 94 and 86 cases, respectively, as well as 77 samples of normal cervix, were immunohistochemically investigated and the results compared with data for expression of oestrogen and progesterone receptors (ER and PR) and c-jun. RT-PCR and western blot assays were also applied to 21 cervical carcinomas and 24 normal tissues. With cervical glandular lesions, significant up-regulation of pS2 expression at both the mRNA and the protein levels was observed for adenocarcinomas in situ (AISs) and overt carcinomas, closely linked with mucinous differentiation and tumour grades. pS2 scores were inversely related to ERalpha status for all cervical glandular categories, while there was no association with ERbeta and PR values. In squamous lesions, pS2 values did not differ between normal and malignant lesions, in contrast to the significant down-regulation of ERalpha expression with tumour development. Although c-jun expression significantly correlated with ERalpha values for all squamous categories, it did not relate to pS2 status in either C-ACas or ISCCs. These results indicate that alterations in pS2 expression may occur relatively early in the development of cervical glandular, but not squamous lesions, independently of factors known to promote transcription of the pS2 gene.
authors.affiliation: Department of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Saegusa
authors.forename: M
authors.initials: M
authors.lastname: Hashimura
authors.forename: A
authors.initials: A
authors.lastname: Hara
authors.forename: I
authors.initials: I
authors.lastname: Okayasu
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000378:metabolism*; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D011506:Proteins / Q000235:genetics / Q000378:metabolism*; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071163:Trefoil Factor-1; D025521:Tumor Suppressor Proteins; D015854:Up-Regulation; D002583:Uterine Cervical Neoplasms / Q000378:metabolism*
chemical_list: D009363:Neoplasm Proteins; D011506:Proteins; D016755:Proto-Oncogene Proteins c-jun; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C051838:TFF1 protein, human; D000071163:Trefoil Factor-1; D025521:Tumor Suppressor Proteins