ArticleJournal of cancer research and clinical oncology2013
KLF8 involves in TGF-beta-induced EMT and promotes invasion and migration in gastric cancer cells.
Article in Journal of cancer research and clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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70 citing papers in PubMed, 100 citations in OpenAlex.
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- The role of circRNAs in resistance to doxorubicin.Cell communication and signaling : CCS · 2024Review
- Krüppel-like factors family in health and disease.MedComm · 2024Review
- Zinc Finger Proteins in the War on Gastric Cancer: Molecular Mechanism and Clinical Potential.Cells · 2023Review
- Cancer-associated fibroblast-secreted IGFBP7 promotes gastric cancer by enhancing tumor associated macrophage infiltration via FGF2/FGFR1/PI3K/AKT axis.Cell death discovery · 2023Article
- Kruppel-like factor 8 regulates triple negative breast cancer stem cell-like activity.Frontiers in oncology · 2023Article
- Kruppel-like Factors in Skeletal Physiology and Pathologies.International journal of molecular sciences · 2022Review
- Regulation of TGF-Cancers · 2022Article
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- lncRNA OGFRP1 promotes tumor progression by activating the AKT/mTOR pathway in human gastric cancer.Aging · 2021Article
- Understanding the Complex Milieu of Epithelial-Mesenchymal Transition in Cancer Metastasis: New Insight Into the Roles of Transcription Factors.Frontiers in oncology · 2021Review
- LncRNA HCP5 : A Potential Biomarker for Diagnosing Gastric Cancer.Frontiers in oncology · 2021Article
- Review
- Serpin peptidase inhibitor clade A member 1-overexpression in gastric cancer promotes tumor progressionOncology letters · 2020Article
- Long non‑coding RNA MEG3 suppresses epithelial‑to‑mesenchymal transition by inhibiting the PSAT1‑dependent GSK‑3β/Snail signaling pathway in esophageal squamous cell carcinoma.Oncology reports · 2020Article
- Distinct prognostic values and antitumor effects of tumor growth factor β1 and its receptors in gastric cancer.Oncology letters · 2020Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeKrüppel-like factor 8 (KLF8), a downstream transcription factor of transforming growth factor-β1 (TGF-β1), has a role in tumorigenesis, tumor progress and epithelial-to-mesenchymal transition (EMT) induction. Recent studies mainly focused on its role in breast cancer and hepatocellular carcinoma; however, little is studied in gastric cancer. Here, we aim to explore whether KLF8 is involved in TGF-β1-induced EMT in gastric cancer cells.
methodsWestern blot and real-time PCR assays were used to detect the expression of KLF8, E-cadherin and vimentin in gastric cancer cell line SGC7901 treated with or without TGF-β1. The lentivirus-mediated RNA interference technique was used to knock down the expression of KLF8 in gastric cancer cell line SGC7901. In vitro, the ability of cell migration and invasion were measured by transwell and wound healing assays; the cell motility was detected by high content screening assay.
resultsTGF-β1 could induce EMT via down-regulating E-cadherin and up-regulating vimentin expression in gastric cancer cells. Further study found that TGF-β1 could induce KLF8 expression at the protein and mRNA levels in gastric cancer cells (P < 0.05). Western blot and real-time PCR assays found that small interference RNA (siRNA)-mediated KLF8 silence blocked TGF-β1-induced EMT-like transformation and subsequently reversed the loss of E-cadherin and gain of vimentin. In vitro, inhibition of KLF8 decreased TGF-β1-prompted cell migration, invasion and motility.
conclusionsKLF8, a transcription factor, is involved in TGF-β1-induced EMT in gastric cancer cells and may be a novel therapeutic target for the treatment of gastric cancer.
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