ArticleOncology letters2016
SIX1 is overexpressed in endometrial carcinoma and promotes the malignant behavior of cancer cells through ERK and AKT signaling.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- AKT inhibitors in gynecologic oncology: past, present and future.Frontiers in oncology · 2025Review
- Phosphorylation determines the glucose metabolism reprogramming and tumor-promoting activity of sine oculis homeobox 1.Signal transduction and targeted therapy · 2024Article
- Targeting sine oculis homeoprotein 1 (SIX1): A review of oncogenic roles and potential natural product therapeutics.Heliyon · 2024Review
- Review
- Endometrial Stem Cells: Orchestrating Dynamic Regeneration of Endometrium and Their Implications in Diverse Endometrial Disorders.International journal of biological sciences · 2024Review
- Manzamine-A Alters In Vitro Calvarial Osteoblast Function.Marine drugs · 2022Article
- High expression of SIX1 is an independent predictor of poor prognosis in endometrial cancer.American journal of translational research · 2021Article
- Article
- MicroRNA-155-3p promotes glioma progression and temozolomide resistance by targeting Six1.Journal of cellular and molecular medicine · 2020Article
- miR-489-3p/SIX1 Axis Regulates Melanoma Proliferation and Glycolytic Potential.Molecular therapy oncolytics · 2020Article
- Identification of EMT-Related Gene Signatures to Predict the Prognosis of Patients With Endometrial Cancer.Frontiers in genetics · 2020Article
- SIX1 Regulates Aberrant Endometrial Epithelial Cell Differentiation and Cancer Latency Following Developmental Estrogenic Chemical Exposure.Molecular cancer research : MCR · 2019Article
- MicroRNA-23a inhibits endometrial cancer cell development by targeting SIX1.Oncology letters · 2019Article
- MicroRNA-362 Inhibits Cell Proliferation and Invasion by Directly Targeting SIX1 in Colorectal Cancer.Yonsei medical journal · 2019Article
- Transcriptional Downregulation of miR-4306 serves as a New Therapeutic Target for Triple Negative Breast Cancer.Theranostics · 2019Article
- microRNA-488 inhibits chemoresistance of ovarian cancer cells by targeting Six1 and mitochondrial function.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sineoculis homeobox homolog 1 (SIX1) protein has been found to be important for cancer progression. However, its biological role in human endometrial carcinomas remains unexplored. The potential mechanism of SIX1-induced cancer progression remains unclear. In the present study, SIX1 protein expression was examined in 84 cases of endometrial carcinoma tissues using immunohistochemisty, and SIX1 was found to be overexpressed in 51.1% (43/84) of cervical cancer cells. Small interfering RNA (siRNA) knockdown of SIX1 was also performed in Ishikawa cells with high endogenous SIX1 expression, and SIX1 was overexpressed in the HEC1B cell line with low endogenous expression. SIX1 overexpression promoted cell growth rate and colony formation ability, whereas SIX1 depletion inhibited cell growth and colony formation. Further analysis showed that SIX1 knockdown downregulated, and SIX1 overexpression upregulated, cyclin D1, cyclin E, phosphorylated (p-)extracellular signal-regulated kinase (ERK), and p-protein kinase B (AKT) expression. The ERK inhibitor, U0126, and AKT inhibitor treatments blocked the effect of SIX1 on proliferation. In conclusion, the present study found that SIX1 overexpression promotes cancer cell growth in endometrial carcinoma, possibly through ERK- and AKT-mediated pathways.
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