ArticleCancer cell international2020
SALL4 promotes gastric cancer progression via hexokinase II mediated glycolysis.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- The evolving landscape of the Warburg effect in gastric cancer: From molecular mechanisms to targeted therapy.Clinical and translational medicine · 2026Review
- Review
- SALL4-targeted therapeutic peptide PEN-FFW suppresses PD-L1 and enhances CD8⁺ T cell cytotoxicity via regulating PI3K/AKT signaling in breast cancer.Immunologic research · 2026Article
- Metabolic Reprogramming in Gastric Cancer Immunity Mechanisms and Therapeutic Implications.Oncology research · 2026Review
- Transcription factor MYB regulates glycolysis to promote the transfer and malignant progression of gastric cancer through the SSBP2/ISL1 axis.Cancer cell international · 2025Article
- Alectinib and SALL4-Targeted Fatty Acid Oxidation: A Strategy to Combat Oxaliplatin Resistance in Gastric Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Molecular mechanisms of metastatic peritoneal dissemination in gastric adenocarcinoma.Cancer metastasis reviews · 2025Review
- Advances in the Study of Metabolic Reprogramming in Gastric Cancer.Cancer medicine · 2025Review
- An in- vitro measurement for the toxicity of peptides inhibit hexokinase II in breast cancer cell lines.Scientific reports · 2025Article
- USP37-stabilized SALL4 promotes the keloid formation by PI3K/AKT pathway.Scientific reports · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- "Friends or foes": a new perspective of tumour metabolic transcriptional modification.Cell death & disease · 2025Review
- Cytoplasmic SALL4-A isoform expression as a diagnostic marker of less aggressive tumor behavior in gastric cancer.World journal of surgical oncology · 2025Article
- Pain, lactate, and anesthetics: intertwined regulators of tumor metabolism and immunity.Frontiers in oncology · 2025Review
- HOXC12 promotes the invasion and migration of gastric cancer cells by upregulating SALL4 and activating Wnt/β-catenin signaling pathway.Discover oncology · 2024Article
- Discovery of Di(het)arylmethane and Dibenzoxanthene Derivatives as Potential Anticancer Agents.International journal of molecular sciences · 2024Article
- Adipose-derived stem cells promote glycolysis and peritoneal metastasis via TGF-β1/SMAD3/ANGPTL4 axis in colorectal cancer.Cellular and molecular life sciences : CMLS · 2024Article
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe stem cell factor SALL4 is reactivated in human cancers. SALL4 plays diverse roles in tumor growth, metastasis, and drug resistance, but its role in tumor metabolism has not been well characterized.
methodsThe glycolytic levels of gastric cancer cells were detected by glucose uptake, lactate production, lactate dehydrogenase activity, ATP level, and hexokinase activity. QRT-PCR and western blot were used to detect the changes in the expression of glycolytic genes and proteins. The downstream target genes of SALL4 were identified by microarray. The regulation of hexokinase II (HK-2) by SALL4 was analyzed by luciferase reporter assay and chromatin immunoprecipitation assay. Transwell migration assay, matrigel invasion assay, cell counting assay and colony formation assay were used to study the roles of HK-2 regulation by SALL4 in gastric cancer cells in vitro. The effects of SALL4 on glycolysis and gastric cancer progression in vivo were determined by subcutaneous xenograft and peritoneal metastasis tumor models in nude mice.
resultsSALL4 knockdown inhibited glucose uptake, lactate production, lactate dehydrogenase activity, ATP level and hexokinase activity in gastric cancer cells, and decreased the expression of glycolytic genes and proteins. Microarray analysis showed that SALL4 knockdown affected glycolysis-related pathway. The regulation of HK-2 gene expression by SALL4 was confirmed by luciferase reporter assay and chromatin immunoprecipitation assay. HK-2 knockdown abrogated the promotion of glycolysis by SALL4 in gastric cancer cells, indicating that HK-2 acts as a downstream effector of SALL4. Moreover, HK-2 knockdown reversed the promoting role of SALL4 in gastric cancer cell proliferation, migration and invasion, suggesting that SALL4 drives gastric cancer progression by upregulating HK-2.
conclusionsSALL4 promotes gastric cancer progression through HK-2-mediated glycolysis, which reveals a new mechanism for the oncogenic roles of SALL4 in cancer.
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