scholarly journals EphrinA1 stimulates cell attachment and inhibits cell aggregation through the EphA receptor pathway in human endometrial carcinoma-derived Ishikawa cells

2011 ◽  
Vol 26 (5) ◽  
pp. 1163-1170 ◽  
Author(s):  
H. Fujii ◽  
H. Fujiwara ◽  
A. Horie ◽  
K. Suginami ◽  
Y. Sato ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Cell Attachment ◽  
Cell Aggregation ◽  
Ishikawa Cells ◽  
Epha Receptor

scholarly journals Bu Shen Yang Xue Prescription Has Treating Effect on Endometrial Cancer through FSH/PI3K/AKT/Gankyrin/HIF-α/cyclinD 1 Pathway in Ishikawa Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Yue-qun Chen ◽  
Hua-li Fei ◽  
Hong-li Zhu
Keyword(s):  
Endometrial Cancer ◽  
Endometrial Carcinoma ◽  
Cancer Cell ◽  
Nude Mice ◽  
Follicle Stimulating Hormone ◽  
Control Group ◽  
Model Group ◽  
Migration Ability ◽  
Ishikawa Cells ◽  
And Migration

Background. The formulation of Bu Shen Yang Xue (BSYX) has been clinically used in treating gynecologic disease in China, especially for the development of the endometrium. Endometrial carcinoma is the most common malignant tumor of the female genital tract in developed countries. And few studies have been reported on the antitumor activity of BSYX. Therefore, this study aimed to investigate the effect of BSYX on endometrial cancer and make an initial discussion of the underlining mechanisms in Ishikawa cells. Methods and Results. Firstly, 60 SPF female nude mice were randomly divided into control group, model group, BSYX group, and positive group. The models of subcutaneous tumor xenograft of nude mice were established by injection of human endometrial carcinoma cell line Ishikawa tumor cell suspension. Compared with model group, BSYX reduced effectively tumor volume and changed pathological feature in mice tumor issue. Meanwhile, proteins from tumor issues were detected by western blot analysis. The protein levels of follicle-stimulating hormone receptor (FSHR), p-Akt/Akt, Gankyrin, and cyclinD1 in the model group were higher than those in control group but the expression in BSYX group was lower than that in the model group. The hypoxia inducible factor alpha (HIF-α) protein level in the model group was lower than those in control group and upregulated in BSYX group. In addition, Ishikawa cells were cultured and then exposed to follicle-stimulating hormone (FSH), LY294002, a highly selective PI3K inhibitor and serum containing BSYX, respectively. LY294002 and BSYX markedly decreased the cancer cell viability and migration ability and increased the apoptosis rate. FSH promoted the cancer cell ability and migration ability. LY294002 and BSYX evidently downregulated the proteins levels of FSHR, p-Akt/Akt, Gankyrin, and cyclinD1 and upregulated the expression of HIF-α protein, and FSH was on the opposite. Conclusions. Taken together, our results showed that the formulation of BSYX had antitumor effect on endometrial cancer in vivo and in vitro and was related with FSH/PI3K/AKT/Gankyrin/HIF-α/cyclinD1 transduction pathway.

scholarly journals Expression of NR1H3 in endometrial carcinoma and its effect on the proliferation of Ishikawa cells in vitro

2019 ◽  
Vol Volume 12 ◽  
pp. 685-697
Author(s):  
Fang Fang ◽  
Dawei Li ◽  
Lu Zhao ◽  
Yue Li ◽  
Teng Zhang ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Ishikawa Cells

scholarly journals 1α,25(OH)2D3 Induces Actin Depolymerization in Endometrial Carcinoma Cells by Targeting RAC1 and PAK1

2016 ◽  
Vol 40 (6) ◽  
pp. 1455-1464 ◽  
Author(s):  
Ni Zeng ◽  
Madhuri S. Salker ◽  
Shaqiu Zhang ◽  
Yogesh Singh ◽  
Bing Shi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Actin Cytoskeleton ◽  
Endometrial Carcinoma ◽  
Actin Polymerization ◽  
Carcinoma Cells ◽  
Filamentous Actin ◽  
Transcript Levels ◽  
Actin Depolymerization ◽  
Protein Levels ◽  
Ishikawa Cells

Background: Cell proliferation and motility require actin reorganization, which is under control of various signalling pathways including ras-related C3 botulinum toxin substrate 1 (RAC1), p21 protein-activated kinase 1 (PAK1) and actin related protein 2 (ARP2). Tumour cell proliferation is modified by 1α,25-Dihydroxy-Vitamin D3 (1α,25(OH)2D3), a steroid hormone predominantly known for its role in calcium and phosphorus metabolism. The present study explored whether 1α,25(OH)2D3 modifies actin cytoskeleton in Ishikawa cells, a well differentiated endometrial carcinoma cell line. Methods: To this end, actin cytoskeleton was visualized by confocal microscopy. Globular over filamentous actin ratio was determined utilizing Western blotting and flow cytometry, transcript levels by qRT-PCR and protein abundance by immunoblotting. Results: A 24 hour treatment with 1α,25(OH)2D3 (100 nM) significantly decreased RAC1 and PAK1 transcript levels and activity, decreased ARP2 protein levels and depolymerized actin. The effect of 1α,25(OH)2D3 on actin polymerization was mimicked by pharmacological inhibition of RAC1 and PAK1. Conclusions: 1α,25(OH)2D3 leads to disruption of RAC1 and PAK1 activity with subsequent actin depolymerization of endometrial carcinoma cells.

scholarly journals Estrogen Up-Regulates Mismatch Repair Activity in Normal and Malignant Endometrial Glandular Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4863-4870 ◽  
Author(s):  
Tsutomu Miyamoto ◽  
Tanri Shiozawa ◽  
Hiroyasu Kashima ◽  
Yu-Zhen Feng ◽  
Akihisa Suzuki ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Mismatch Repair ◽  
Proliferating Cells ◽  
Endometrial Cells ◽  
Estrogen Exposure ◽  
Estrogen Receptor Positive ◽  
Ishikawa Cells ◽  
Glandular Cells ◽  
Repair Activity

Impaired mismatch repair (MMR) is reportedly crucial in the early stages of endometrial carcinogenesis. Although estrogen exposure is considered an important risk factor for endometrial carcinoma, the relationship between estrogen and MMR activity remains undetermined. The present study was undertaken to elucidate the effect of estrogen on MMR activity in normal and malignant endometrial cells. The expression of MMR proteins, hMLH1 and hMSH2, and its correlation with estrogen was examined using immunohistochemical and immunofluorescent techniques. The effect of estradiol (E2) on the expression of hMLH1/hMSH2 protein/mRNA and in vitro MMR activity using two types of heteroduplex (G/T mismatches, 2-base insertion-deletion loops) was examined in cultured normal endometrial glandular cells and estrogen receptor-positive endometrial carcinoma Ishikawa cells. Immunohistochemical expression of hMLH1 and hMSH2 in normal endometrial glands was positively correlated with the serum E2 levels. The expression of hMLH1/hMSH2 protein and mRNA was increased in normal endometrial glandular and Ishikawa cells by E2 treatment. In vitro MMR activity was up-regulated by E2 in both types of cell and heteroduplex. Immunofluorescent analysis demonstrated that E2 enhanced proliferation and hMLH1/hMSH2 expression in both cells; however, proliferating cells without hMLH1/hMSH2 expressions implying high-risk cells were more frequently observed under low E2 concentrations. Collectively, the E2-induced up-regulation of MMR activity in endometrial cells suggests that high estrogen levels act as an intrinsic defense against endometrial carcinogenesis, whereas the imbalance between cell growth and MMR under low E2 environment as seen at postmenopause is vulnerable to carcinogenesis.

scholarly journals NCAM polysialic acid can regulate both cell-cell and cell-substrate interactions.

1991 ◽  
Vol 114 (1) ◽  
pp. 143-153 ◽  
Author(s):  
A Acheson ◽  
J L Sunshine ◽  
U Rutishauser
Keyword(s):  
Tissue Culture ◽  
Cell Attachment ◽  
Surface Membrane ◽  
Polysialic Acid ◽  
Cell Aggregation ◽  
Important Variable ◽  
Substrate Interactions ◽  
Cell Substrate ◽  
Culture Models ◽  
Cell Cell

We have proposed previously that the polysialic acid (PSA) moiety of NCAM can influence membrane-membrane apposition, and thereby serve as a selective regulator of a variety of contact-dependent cell interactions. In this study, cell and tissue culture models are used to obtain direct evidence that the presence of PSA on the surface membrane can affect both cell-cell and cell-substrate interactions. Using a neuroblastoma/sensory neuron cell hybrid, it was found that removal of PSA with a specific neuraminidase (endo-N) augments cell-cell aggregation mediated by the L1 cell adhesion molecule as well as cell attachment to a variety of tissue culture substrates. In studies of embryonic spinal cord axon bundling, which involves both cell-cell and cell-substrate interactions, the pronounced defasciculation produced by removal of PSA is most easily explained by an increase in cell-substrate interaction. The fact that in both studies NCAM's intrinsic adhesion function was found not to be an important variable further illustrates that regulation of the cell surface by PSA can extend beyond binding mediated by the NCAM polypeptide.

2Fibulin-5 Inhibits Proliferation of Endometrial Carcinoma Ishikawa Cells by Down-Regulating β-Catenin

2020 ◽  
Vol 10 (2) ◽  
pp. 189-194
Author(s):  
Jing Chu ◽  
Zhichao Tong ◽  
Xiaolan Zhou ◽  
Teng Li
Keyword(s):  
Endometrial Cancer ◽  
Cell Viability ◽  
Endometrial Carcinoma ◽  
Cancer Cell Proliferation ◽  
Ishikawa Cells ◽  
Cancer Tissues ◽  
Related Pathway ◽  
Tissue Cancer

Endometrial cancer is a malignance in the uterus. The incidence of endometrial cancer is increasing recent years. Fibulin-5 participates in tissue homeostasis. The exact role of Fibulin-5 in endometrial cancer, such as becoming a sensitive tumor marker for endometrial cancer for diagnosis and follow-up, remains to be determined. 30 cases of endometrial tissue cancer specimens and adjacent tissues were collected for analysis of the expression of Fibulin-5 by western blot. Endometrial carcinoma Ishikawa cells (ECICs) were cultured and the level of Fibulin-5 was regulated via transfection. β-catenin level was measured followed by analysis of cell viability by MTT assay or BrdU staining. Results showed that Fibulin-5 in endometrial carcinoma tissues was significantly downregulated compared to para cancer tissues. Overexpression of Fibulin-5 decreased cell viability of endometrial carcinoma Ishikawa cells (ECICs) whereas downregulation increased cell viability. Meanwhile, Fibulin-5 overexpression significantly downregulated β-catenin and β-catenin knockdown blocked the proliferation effect caused by Fibulin-5 on ECICs. In conclusion, Fibulin-5 could inhibit cancer cell proliferation possibly via β-catenin related pathway.

scholarly journals Autocrine stimulation of IGF1 in estrogen-induced growth of endometrial carcinoma cells: involvement of the mitogen-activated protein kinase pathway followed by up-regulation of cyclin D1 and cyclin E

2009 ◽  
Vol 16 (1) ◽  
pp. 113-122 ◽  
Author(s):  
Hiroyasu Kashima ◽  
Tanri Shiozawa ◽  
Tsutomu Miyamoto ◽  
Akihisa Suzuki ◽  
Junko Uchikawa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Cyclin D1 ◽  
Endometrial Carcinoma ◽  
Carcinoma Cells ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Ishikawa Cells ◽  
Autocrine Stimulation ◽  
Stimulation Of

To examine estrogen-induced growth mechanisms of endometrial carcinoma, we investigated the estrogen-induced activation of the mitogen-activated protein kinase (MAPK) pathway and cell cycle regulators. Estradiol (E2) treatment at concentrations of 10−8 M and 10−6 M to estrogen receptor (ER)-positive endometrial carcinoma Ishikawa cells for 24 h resulted in increased cell proliferation by 20% and 28% respectively. The E2-induced proliferation was associated with the activation of extracellular signal-regulated kinase (MAPK)3/1 and up-regulation of cyclin D1 and E, which were suppressed by the addition of an MAP2K inhibitor (U0126) or an ER antagonist (ICI 182 780). Then, our screening for estrogen-inducible growth factors identified that IGF1 was up-regulated remarkably by E2. Immunoprecipitation using conditioned medium of Ishikawa cells after E2 treatment confirmed the E2-induced secretion of IGF1 protein. Treatment with recombinant IGF1 stimulated cell proliferation in a dose-dependent fashion, in association with MAPK3/1 phosphorylation and up-regulation of cyclin D1 and E. These IGF1-induced responses were suppressed by treatment with MAP2K inhibitor or anti-IGF1 receptor antibody. Immunohistochemical staining confirmed the expression of activated MAPK3/1 in normal proliferative phase endometria and endometrial carcinomas, indicating the involvement of this pathway in actively proliferating endometrial tissues in vivo. These findings suggest that E2-induced proliferation of endometrial carcinoma cells is mediated by the MAPK3/1 pathway via autocrine stimulation of IGF1.

scholarly journals Estrogen/estrogen receptor promotes the proliferation of endometrial carcinoma cells by enhancing hMOF expression

2020 ◽  
Vol 50 (3) ◽  
pp. 241-253 ◽  
Author(s):  
Yue Qi ◽  
Mingzi Tan ◽  
Mingjun Zheng ◽  
Shan Jin ◽  
Huimin Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Estrogen Receptor ◽  
Endometrial Carcinoma ◽  
Cell Apoptosis ◽  
Carcinoma Cells ◽  
Signalling Pathways ◽  
Migration And Invasion ◽  
Cell Cycle Distribution ◽  
Reaction Cell ◽  
Ishikawa Cells

Abstract Background This study aims to analyse the expression of human MOF in endometrial carcinoma cells and its relationship with estrogen and estrogen receptor and to investigate the effect of estrogen–human MOF on the malignant biological behaviours of endometrial carcinoma cells. Methods The expression of human MOF was detected in different endometrial tissues by immunohistochemistry. The effects of human MOF, human MOF combined with estrogen stimulation and estrogen plus anti-human MOF antibody blocking on the proliferation of endometrial carcinoma cells were evaluated by western blotting, real-time polymerase chain reaction, cell proliferation assay and cell cycle distribution. Bioinformatics was used to identify the correlations of human MOF and estrogen and involved pathways. Results The expression levels of human MOF in endometrial carcinoma tissues were significantly higher than that in atypical hyperplasia and normal endometrial tissues. High expression of human MOF was associated with late-stage cancer, lymph node metastasis and short survival time, and it was also an independent prognostic risk factor for endometrial carcinoma. After human MOF knockdown, the proliferation, migration and invasive capacity of Ishikawa cells decreased and cell apoptosis increased. After stimulation with estrogen, the PI3K/Akt and Ras–Raf–MEK–ERK signalling pathways were activated, and the expression of the human MOF protein was increased. human MOF (KAT8) expression showed a positive correlation with ESR1 expression, and KAT8-associated genes were enriched in the cell cycle pathways and splicing pathways. Conclusion Human MOF was highly expressed in endometrial carcinoma and associated with proliferation. Estrogen/estrogen receptor enhanced human MOF expression; promoted the proliferation, migration and invasion of Ishikawa cells; and inhibited cell apoptosis by activating the PI3K/Akt and Ras–Raf–MEK–ERK signalling pathways.

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