Abstract
BackgroundCaveolin-1 (CAV1) has been implicated both in tumor suppression and progression, whereby the specific role appears to be context dependent. Endometrial cancer is one of the most common malignancies of the female genital tract; however, little is known about the role of CAV1 in this disease.MethodsHere, we first determined by immunohistochemistry CAV1 protein levels in normal proliferative human endometrium and endometrial tumor samples. Then using two endometrial cancer cell lines (ECC: Ishikawa and Hec-1A) we evaluated mRNA and protein levels of CAV1 by real time qPCR and Western blot analysis, respectively. The role of CAV1 expression in ECC malignancy was further studied by either inducing its expression in endometrial cancer cells with the tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (4β-TPA) or decreasing expression using short-hairpin RNA constructs, and then evaluating the effects of these changes on ECC proliferation, transmigration, matrigel invasion, and colony formation in soft agar.ResultsImmunohistochemical analysis of endometrial epithelia revealed that substantially higher levels of CAV1 were present in endometrial tumors than the normal proliferative epithelium. Also, in Ishikawa and Hec-1A endometrial cancer cells CAV1 expression was readily detectable. Upon treatment with 4β-TPA CAV1 levels increased and coincided with augmented cell transmigration, matrigel invasion, as well as colony formation in soft agar. Reduction of CAV1 expression using short-hairpin RNA constructs ablated these effects in both cell types whether treated or not with 4β-TPA. Alternatively, CAV1 expression appeared not to modulate significantly proliferation of these cells.ConclusionOur study shows that elevated CAV1, observed in patients with endometrial cancer, is linked to enhanced malignancy of endometrial cancer cells, as evidenced by increased migration, invasion and anchorage-independent growth.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1477-5) contains supplementary material, which is available to authorized users.
Highlights
Caveolin-1 (CAV1) has been implicated both in tumor suppression and progression, whereby the specific role appears to be context dependent
We show that CAV1 was expressed at low levels in normal proliferating endometrium, but was readily detectable in endometrial samples of human adenocarcinomas of tumor grades 1-3, as well as in endometrial cancer cells (ECC) lines
In hyperplasia, which is characterized by increased proliferation of the endometrial epithelial cells, CAV1 expression was elevated in the glandular epithelium and remained increased in the different stages of endometrial tumor progression compared to normal proliferative endometrium (NPE) (Fig. 1a and b)
Summary
Caveolin-1 (CAV1) has been implicated both in tumor suppression and progression, whereby the specific role appears to be context dependent. Endometrial cancer is one of the most common malignancies of the female genital tract; little is known about the role of CAV1 in this disease. Endometrial adenocarcinoma is one of the most common malignancies of the female genital tract [14] and is considered a very frequent tumor type in industrialized countries [15]. Little is known about CAV1 in this type of cancer compared with others, like breast cancer [16,17,18,19,20]. In a microarray study of type I endometrial cancer biopsies, a decrease in CAV1 mRNA was reported when compared with control samples [22]. Whether CAV1 is expressed and how the protein may contribute to the development of endometrial cancer remains an open question
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