ArticleScientific reports2018
GRAMD1B regulates cell migration in breast cancer cells through JAK/STAT and Akt signaling.
Article in Scientific reports, 2018. 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, 52 citations in OpenAlex.
- Role of STAT3 signaling pathway in breast cancer.Cell communication and signaling : CCS · 2020Pooled it
- Organelle contact sites in cancer cells.Cell death & disease · 2026Review
- Enhanced early detection of thyroid cancer using ensemble machine learning and serum proteomics.Frontiers in oncology · 2026Article
- The involvement of exosomes in the tumorigenicity of breast cancer cell lines through the crosstalk between STAT3, Notch, and Wnt signaling pathways.Discover oncology · 2025Article
- GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau.Nature communications · 2025Article
- Targeting the Key Signaling Pathways in Breast Cancer: From Molecular Mechanism to Therapeutic Interventions.Recent patents on anti-cancer drug discovery · 2025Review
- Analysis of Endoplasmic Reticulum Stress-Associated Proteins As Prognostic Markers In Breast Cancer.Current genomics · 2025Article
- Transcriptome insights into newcastle disease virus-mediated eradication of cholangiocarcinoma cells.PloS one · 2025Article
- Examining genotype-phenotype associations of GRAM domain proteins using GWAS, PheWAS and literature review in cattle, human, pig, mouse and chicken.Scientific reports · 2024Article
- Knocking down GRAMD1C expression reduces 6-OHDA-induced apoptosis in PC12 cells.Toxicology research · 2024Article
- Article
- Potential therapeutic targets of the JAK2/STAT3 signaling pathway in triple-negative breast cancer.Frontiers in oncology · 2024Review
- MiR-4646-5p Acts as a Tumor-Suppressive Factor in Triple Negative Breast Cancer and Targets the Cholesterol Transport Protein GRAMD1B.Non-coding RNA · 2023Article
- Crocin exerts anti-tumor effect in colon cancer cells <em>via</em> repressing the JAK pathway.European journal of histochemistry : EJH · 2023Article
- The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer.Molecular cancer · 2023Article
- Review
- Identifying the Transcriptional Drivers of Metastasis Embedded within Localized Melanoma.Cancer discovery · 2023Article
- Construction of a 5-gene prognostic signature based on oxidative stress related genes for predicting prognosis in osteosarcoma.PloS one · 2023Article
- A Whole-Genome Sequencing Study Implicates GRAMD1B in Multiple Sclerosis Susceptibility.Genes · 2022Article
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated JAK/STAT signaling has been implicated in breast cancer metastasis, which is associated with high relapse risks. However, mechanisms underlying JAK/STAT signaling-mediated breast tumorigenesis are poorly understood. Here, we showed that GRAMD1B expression is upregulated on IL-6 but downregulated upon treatment with the JAK2 inhibitor AG490 in the breast cancer MDA-MB-231 cells. Notably, Gramd1b knockdown caused morphological changes of the cells, characterized by the formation of membrane ruffling and protrusions, implicating its role in cell migration. Consistently, GRAMD1B inhibition significantly enhanced cell migration, with an increase in the levels of the Rho family of GTPases. We also found that Gramd1b knockdown-mediated pro-migratory phenotype is associated with JAK2/STAT3 and Akt activation, and that JAK2 or Akt inhibition efficiently suppresses the phenotype. Interestingly, AG490 dose-dependently increased p-Akt levels, and our epistasis analysis suggested that the effect of JAK/STAT inhibition on p-Akt is via the regulation of GRAMD1B expression. Taken together, our results suggest that GRAMD1B is a key signaling molecule that functions to inhibit cell migration in breast cancer by negating both JAK/STAT and Akt signaling, providing the foundation for its development as a novel biomarker in breast cancer.
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