Observational studyCancer science2021
Expression of asporin reprograms cancer cells to acquire resistance to oxidative stress.
Observational study in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 28 citations in OpenAlex.
- Coordinated Immune Activation Following KRAS Inhibition in Syngeneic Models Reveals Molecular Pathways that Potentiate and Limit Antitumor Immunity.Cancer immunology research · 2026Article
- Asporin promotes gastric cancer progression by regulating NRF2 ubiquitination and competitively binding to KEAP1.Translational cancer research · 2026Article
- Asporin regulates glycolysis and stemness of gastric cancer cells.Journal of molecular histology · 2026Article
- From stasis to systematics: deciphering the pathophysiology of secondary lymphedema through omics.Frontiers in immunology · 2026Review
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway.Cell death & disease · 2025Article
- Comparison of Differentially Expressed Genes in Human and Canine Osteosarcoma.Life (Basel, Switzerland) · 2025Article
- Integrating multiomics analysis and machine learning to refine the molecular subtyping and prognostic analysis of stomach adenocarcinoma.Scientific reports · 2025Article
- Revealing Potential Therapeutic Targets in Gastric Cancer through Inflammation and Protein-Protein Interaction Hub Networks.Journal of Cancer · 2025Article
- Mitochondria: a new intervention target for tumor invasion and metastasis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Advances in targeting cancer-associated fibroblasts through single-cell spatial transcriptomic sequencing.Biomarker research · 2024Review
- Molecular analysis of primary and metastatic sites in patients with renal cell carcinoma.The Journal of clinical investigation · 2024Article
- 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
- ASPORIN: A root of the matter in tumors and their host environment.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- Exosomes secreted by ST3GAL5Molecular oncology · 2024Article
- Bone marrow adipocytes induce cancer-associated fibroblasts and immune evasion, enhancing invasion and drug resistance.Cancer science · 2023Article
- Landscape of Druggable Molecular Pathways Downstream of Genomic CDH1/Cadherin-1 Alterations in Gastric Cancer.Journal of personalized medicine · 2022Article
- Persistent Properties of a Subpopulation of Cancer Cells Overexpressing the Hedgehog Receptor Patched.Pharmaceutics · 2022Article
- Identification of Hub Diagnostic Biomarkers and Candidate Therapeutic Drugs in Heart Failure.International journal of general medicine · 2022Article
- Transcriptomics and Metabolomics Identify Drug Resistance of Dormant Cell in Colorectal Cancer.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Asporin (ASPN), a small leucine-rich proteoglycan expressed predominantly by cancer associated fibroblasts (CAFs), plays a pivotal role in tumor progression. ASPN is also expressed by some cancer cells, but its biological significance is unclear. Here, we investigated the effects of ASPN expression in gastric cancer cells. Overexpression of ASPN in 2 gastric cancer cell lines, HSC-43 and 44As3, led to increased migration and invasion capacity, accompanied by induction of CD44 expression and activation of Rac1 and MMP9. ASPN expression increased resistance of HSC-43 cells to oxidative stress by reducing the amount of mitochondrial reactive oxygen species. ASPN induced expression of the transcription factor HIF1α and upregulated lactate dehydrogenase A (LDHA) and PDH-E1α, suggesting that ASPN reprograms HSC-43 cells to undergo anaerobic glycolysis and suppresses ROS generation in mitochondria, which has been observed in another cell line HSC-44PE. By contrast, 44As3 cells expressed high levels of HIF1α in response to oxidant stress and escaped apoptosis regardless of ASPN expression. Examination of xenografts in the gastric wall of ASPN
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.