ArticleScientific reports2017
SATB2/β-catenin/TCF-LEF pathway induces cellular transformation by generating cancer stem cells in colorectal cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Loss of SATB2 in colorectal cancer is associated with inferior survival and adverse clinicopathologic features: a meta-analysis.American journal of clinical pathology · 2026Pooled it
- EN2 Regulates Pancreatic Cancer Initiation, Progression, and Epithelial-Mesenchymal Transition Through the Notch Signalling Pathway.Journal of cellular and molecular medicine · 2026Article
- Article
- Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer.Oncotarget · 2025Article
- Decoding the role of cancer stem cells in digestive tract tumors: Mechanisms and therapeutic implications (Review).International journal of oncology · 2025Review
- Reduced Expression of SATB2 in Colorectal Cancer and Its Association with Demographic and Clinicopathological Parameters.International journal of molecular sciences · 2025Article
- Assessing the diagnostic potential of SATB2 and β-catenin as biomarkers and therapeutic targets in pancreatic ductal adenocarcinoma.Journal of cancer research and clinical oncology · 2025Article
- SATB2 is an Emergent Biomarker of Anaplastic Thyroid Carcinoma: A Series with Comprehensive Biomarker and Molecular Studies.Endocrine pathology · 2024Article
- Article
- Clinical significance of PNO1 as a novel biomarker and therapeutic target of hepatocellular carcinoma.Journal of cellular and molecular medicine · 2024Article
- Adiponectin-mediated promotion of CD44 suppresses diabetic vascular inflammatory effects.iScience · 2023Article
- Article
- Inhibition of ribosome assembly factor PNO1 by CRISPR/Cas9 technique suppresses lung adenocarcinoma and Notch pathway: Clinical application.Journal of cellular and molecular medicine · 2023Article
- FAK downregulation suppresses stem-like properties and migration of human colorectal cancer cells.PloS one · 2023Article
- Breast mass as the first sign of metastasis from rectal carcinoma: a case report and review of the literature.Frontiers in oncology · 2023Article
- Chronic alcohol exposure induces hepatocyte damage by inducing oxidative stress, SATB2 and stem cell-like characteristics, and activating lipogenesis.Journal of cellular and molecular medicine · 2022Article
- Ethanol exposure of human pancreatic normal ductal epithelial cells induces EMT phenotype and enhances pancreatic cancer development in KC (Pdx1-Cre and LSL-KrasJournal of cellular and molecular medicine · 2022Article
- Increased ACTL6A occupancy within mSWI/SNF chromatin remodelers drives human squamous cell carcinoma.Molecular cell · 2021Article
- Ring finger 220 promotes the stemness and progression of colon cancer cells via Ubiquitin specific peptidase 22-BMI1 axis.Bioengineered · 2021Article
- Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have demonstrated the involvement of colorectal cancer (CRC) stem cells (CSC) in transformation, cancer progression and metastasis. The main goal of this paper was to examine the molecular mechanisms by which SATB2 induced malignant transformation of colorectal epithelial cells. SATB2 induced malignant transformation and these transformed cells gained the characteristics of CSCs by expressing stem cell markers (CD44, CD133, LGR5 and DCLK1) and transcription factors (c-Myc, Nanog and Sox2). Overexpression of SATB2 in normal colorectal epithelial cells increased cell motility, migration and invasion, which were associated with an increase in N-cadherin and Zeb1, and decrease in E-cadherin expression. SATB2 overexpression also upregulated XIAP and cyclin D1, suggesting its role in cell survival and cell cycle. Furthermore, the expression of SATB2 was positively correlated with β-catenin expression in CRC. In contrary, depletion of SATB2 inhibited cell proliferation, colony formation, cell motility and expression of β-catenin, Snail, Slug, Zeb1 and N-cadherin, and upregulated E-cadherin. Furthermore, SATB2 silencing inhibited the expression of stem cell markers, pluripotency maintaining transcription factors, cell cycle and cell proliferation/survival genes and TCF/LEF targets. Finally, β-catenin/TCF-LEF pathway mediated the biological effects of SATB2 in CSCs. These studies support the role of SATB2/β-catenin/TCF-LEF pathway in transformation and carcinogenesis.
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