Establishment of human endometrial adenocarcinoma cell line containing estradiol-17β and progesterone receptors

Ishiwata, Isamu; Ishiwata, Chieko; Soma, C.T. Masayuki; Arai, Junichi; Ishikawa, Hiroshi

doi:10.1016/0090-8258(84)90212-9

Cited by 85 publications

(45 citation statements)

References 18 publications

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“…Therefore, we hypothesized that restoring high miR-145 expression in breast cancer cells may induce a more benign phenotype through downregulation of key molecules involved in breast cancer pathogenesis. We increased miR-145 expression in a panel of wellestablished breast cancer cell lines of varying degree of de-differentiation and malignant potential (Lacroix and Leclercq, 2004), and in an endometrial carcinoma cell line (Ishiwata et al, 1984) by transient microRNA precursor transfection to study the impact of miR-145 overexpression on cell proliferation, motility and invasiveness. miR-145 expression was determined by quantitative real-time PCR in the cell lines MCF-7 (luminal-epithelial-like, estrogen-receptor positive (ER þ ), weakly invasive in vitro), SK-BR-3 (weakly luminal epithelial-like, ERÀ, weakly invasive), MDA-MB-468 (weakly luminal epithelial-like, intermediate invasiveness, ERÀ, forms tumors in nude mice), MDA-MD-231 (mesenchymal morphology, ERÀ, highly invasive and tumorigenic in nude mice) and Ishikawa (endometrial carcinoma, weakly invasive).…”

Section: Resultsmentioning

confidence: 99%

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

et al. 2010

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Micro RNAs are small non-coding RNAs, which regulate fundamental cellular and developmental processes at the transcriptional and translational level. In breast cancer, miR-145 expression is downregulated compared with healthy control tissue. As several predicted targets of miR-145 potentially regulate cell motility, we aimed at investigating a potential role for miR-145 in breast cancer cell motility and invasiveness. Assisted by Affymetrix array technology, we demonstrate that overexpression of miR-145 in MDA-MB-231, MCF-7, MDA-MB-468 and SK-BR-3 breast cancer cells and in Ishikawa endometrial carcinoma cells leads to a downregulation of the cell-cell adhesion protein JAM-A and of the actin bundling protein fascin. Moreover, podocalyxin and Serpin E1 mRNA levels were downregulated, and gamma-actin, transgelin and MYL9 were upregulated upon miR-145 overexpression. These miR-145-dependent expression changes drastically decreased cancer cell motility, as revealed by time-lapse video microscopy, scratch wound closure assays and matrigel invasion assays. Immunofluorescence microscopy demonstrated restructuring of the actin cytoskeleton and a change in cell morphology by miR-145 overexpression, resulting in a more cortical actin distribution, and reduced actin stress fiber and filopodia formation. Nuclear rotation was observed in 10% of the pre-miR-145 transfected MDA-MB-231 cells, accompanied by a reduction of perinuclear actin. Luciferase activation assays confirmed direct miR-145-dependent regulation of the 3 0 UTR of JAM-A, whereas siRNA-mediated knockdown of JAM-A expression resulted in decreased motility and invasiveness of MDA-MB-231 and MCF-7 breast cancer cells. Our data identify JAM-A and fascin as novel targets of miR-145, firmly establishing a role for miR-145 in modulating breast cancer cell motility. Our data provide a rationale for future miR-145-targeted approaches of antimetastatic cancer therapy.

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Section: Resultsmentioning

confidence: 99%

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

et al. 2010

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“…Since Musashi-1 is a stem cell marker, we initially characterized the established Ishikawa cell line 9 for the presence of a cancer stem cell pool, using the Hoechst dye exclusion phenotype 12 and an assay for ALDH-1 activity 14 as surrogate markers for stem cell enrichment. Both SP cells and ALDH-1 positive cells were identified in the Ishikawa cell line, suggesting the presence of putative cancer stem cells.…”

Section: Discussionmentioning

confidence: 99%

“…Ishikawa cells 9 were a generous gift of Dr. Anna StarzinskiPowitz, Frankurt a.M., Germany. The cells were grown in DMEM medium supplemented with 10% fetal calf serum, 2 mmol/L L-glutamine, penicillin and streptomycin in an atmosphere containing 7.5% CO 2 .…”

Section: Cell Culturementioning

confidence: 99%

“…In our study, we investigated the influence of siRNA mediated Musashi-1 knockdown on gene and protein expression of key regulators of the Notch-1 signaling pathway and cell cycle progession using the established human endometrial adenocarcinoma cell line Ishikawa. 9 Furthermore, we determined the stem cell proportion in this cell line by SP analysis and ALDH-1 activity measurements.…”

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confidence: 99%

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The adult stem cell marker Musashi‐1 modulates endometrial carcinoma cell cycle progression and apoptosis via Notch‐1 and p21^WAF1/CIP1

Götte

Greve

Kelsch

et al. 2011

Intl Journal of Cancer

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The RNA-binding protein Musashi-1 has been proposed to maintain stem cell function during development and regenerative processes as a modulator of the Notch-1 signaling pathway. Musashi-1 expression is upregulated in endometrial carcinoma, however, its pathogenetic role in this tumor entity is unknown. Here we investigate the functional impact and mode of action of Musashi-1 on endometrial carcinoma cell behaviour in vitro. Aldehyde dehydrogenase-1 activity and side population (SP) measurement by Hoechst dye exclusion revealed that the Ishikawa endometrial carcinoma cell line contains a pool of putative cancer stem cells. Musashi-1 expression is 20.8-fold upregulated in SP1 compared to SP-and equally distributed between ALDH1 and ALDH-cell pools. siRNA-mediated knockdown of Musashi-1 mRNA expression lead to an altered expression of the signaling receptor Notch-1 and its downstream targets, the transcription factor Hes-1 and the cell cycle regulators p21and cyclin B1, as determined by Western blotting and quantitative real-time PCR. Flow cytometric and ELISA analyses revealed that Musashi-1-mediated modulation of these factors exerted an antiproliferative effect on the cell cycle, and increased apoptosis in endometrial carcinoma cells. We conclude that Ishikawa cells contain a subpopulation of cells with stem cell-like properties. Musashi-1 modulates endometrial carcinoma cell cycle progression and apoptosis via the stemness-related factors Notch-1, Hes-1 and p21 WAF1/CIP1 , thus emerging as a novel future target for endometrial carcinoma therapy.Similar to stem cells, a subpopulation of cancer cells is characterized by a high proliferative capacity, self-renewal, expression of multidrug-resistance proteins, and a high degree of plasticity.

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“…So far, we have found stimulatory and inhibitory activities of the physiological dose of GnRH on the colony-formation of cells using an originally established method, the colony-forming efficiency assay (Enomoto et al ., 2001 and2004a, b). The experimental models used in our studies are TSU-Pr1 (from human prostatic carcinoma, Iizumi et al ., 1987), Jurkat (from human mature leukemia, Gills and Watson, 1980), DU145 (from human prostatic carcinoma, Mickey et al ., 1977;Stone et al ., 1978), and HHUA (from human endometrial carcinoma, Ishiwata et al ., 1984) cell lines. Recently, interesting findings about the mechanisms of the two opposite effects of GnRH have been obtained by adaptation of the technique of RNA interference to our original assay system (Enomoto et al ., 2004b).…”

Section: Introductionmentioning

confidence: 99%

Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

et al. 2004

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Establishment of human endometrial adenocarcinoma cell line containing estradiol-17β and progesterone receptors

Cited by 85 publications

References 18 publications

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

The adult stem cell marker Musashi‐1 modulates endometrial carcinoma cell cycle progression and apoptosis via Notch‐1 and p21^WAF1/CIP1

Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

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Establishment of human endometrial adenocarcinoma cell line containing estradiol-17β and progesterone receptors

Cited by 85 publications

References 18 publications

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

miR-145-dependent targeting of Junctional Adhesion Molecule A and modulation of fascin expression are associated with reduced breast cancer cell motility and invasiveness

The adult stem cell marker Musashi‐1 modulates endometrial carcinoma cell cycle progression and apoptosis via Notch‐1 and p21WAF1/CIP1

Human Type II GnRH Receptor Mediates Effects of GnRH on Cell Proliferation

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The adult stem cell marker Musashi‐1 modulates endometrial carcinoma cell cycle progression and apoptosis via Notch‐1 and p21^WAF1/CIP1