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Targeting SALL4 by Entinostat Inhibits the Malignant Phenotype of Gastric Cancer Cells by Reducing EMT Signaling
Linlin DU1, Fei Xie1, Haibo Han2
1Faculty of Environment and Life, Beijing University of Technology, Beijing, P.R. China.
Background/Aim:
Spalt-like transcription factor 4 (SALL4), as a proto-oncogene, is expressed in various tumors and correlates with poor prognosis of patients. Entinostat, a histone deacetylase (HDAC) inhibitor, has emerged as a potentially promising anti-cancer drug. This study aims to explore the biological role and underlying mechanism of SALL4 targeting by entinostat in gastric cancer.
Materials And Methods:
Online databases were used to exam the link between SALL4 and prognosis. We tested the biological roles of SALL4 in gastric cancer cells. Cell viability and growth were analyzed using the Cell Counting Kit-8 (CCK-8) assay and clone formation assay. Cell migration was assessed using the wound healing assay. The effects of entinostat on gastric cancer cell lines were measured by the CCK-8 assay, clone formation assay, wound healing assay and transwell assay. Epithelial-mesenchymal transition (EMT) signaling pathways were detected by western blot.
Results:
SALL4 expression was upregulated in gastric cancer tissues and positively correlated with tumor stage and prognosis of patients by TCGA dataset analysis. Knockdown of SALL4 by siRNA inhibited the proliferation and migration of gastric cancer cells. In contrast, SALL4 overexpression by stably transfecting a SALL4-expressing plasmid promoted the proliferation and invasiveness of gastric cancer cells in vitro through alteration of EMT-related genes. In addition, entinostat, a HDAC inhibitor targeting SALL4, could suppress the proliferation, migration, and invasion of gastric cancer cells via regulating expression of EMT-associated proteins.
Conclusion:
SALL4 may be a new therapeutic target for the treatment of gastric cancer, and entinostat is a potential novel agent for the treatment of gastric cancer partially by targeting SALL4.
Insights
Spalt-like transcription factor 4 (SALL4) drives gastric cancer progression and poor prognosis. The histone deacetylase inhibitor entinostat targets SALL4, suppressing tumor cell proliferation, migration, and invasion, indicating potential therapeutic applications.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Spalt-like transcription factor 4 (SALL4) is a proto-oncogene implicated in various cancers, correlating with poor patient prognosis.
- Histone deacetylase (HDAC) inhibitors, such as entinostat, represent a promising class of anti-cancer drugs.
Purpose of the Study:
- To investigate the biological role of SALL4 in gastric cancer.
- To elucidate the mechanism by which entinostat targets SALL4 in gastric cancer.
- To evaluate SALL4 as a therapeutic target and entinostat as a potential treatment agent.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) dataset for SALL4 expression and patient prognosis.
- In vitro studies using gastric cancer cell lines to assess SALL4's role in proliferation, migration, and invasion (CCK-8, clone formation, wound healing, Transwell assays).
- Western blot analysis to detect epithelial-mesenchymal transition (EMT) signaling pathways.
Main Results:
- SALL4 is upregulated in gastric cancer tissues and associated with advanced tumor stage and poorer prognosis.
- SALL4 knockdown inhibited gastric cancer cell proliferation and migration, while SALL4 overexpression promoted proliferation and invasiveness.
- Entinostat suppressed gastric cancer cell proliferation, migration, and invasion by regulating EMT-associated proteins, partially through SALL4 targeting.
Conclusions:
- SALL4 represents a potential novel therapeutic target for gastric cancer treatment.
- Entinostat shows promise as a novel therapeutic agent for gastric cancer, partly by targeting SALL4.
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