ArticleOncology research2023
GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling.
Article in Oncology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Epigallocatechin gallate is associated with PDGFRB downregulation and altered PI3K-AKT signaling in gastric cancer.Translational cancer research · 2026Article
- GIPC1 governed ferroptosis by regulating DECR1-modulating lipid homeostasis during dilated cardiomyopathy (DCM).Cell death and differentiation · 2026Article
- Identification of PI3K/AKT/mTOR-related genes as diagnostic biomarkers for cutaneous squamous cell carcinoma.Biochemistry and biophysics reports · 2026Article
- GIPC1 Restrains the Progression and Chemoresistance of Colorectal Cancer by Regulating TTC7B/mTOR/NF-κB Axis.International journal of biological sciences · 2026Article
- Article
- Lipid Nanoparticle-Mediated RNAi Against GIPC1 Overcomes Chemoresistance in Pancreatic Ductal Adenocarcinoma.Pharmaceutics · 2025Article
- HEG1 promotes gastric cancer progression by stabilizing AKT1 and is functionally regulated by the deubiquitinase USP48.European journal of medical research · 2025Article
- Loss ofLife (Basel, Switzerland) · 2025Article
- Stearoylation cycle regulates the cell surface distribution of the PCP protein Vangl2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of Potential Feature Genes in CRSwNP Using Bioinformatics Analysis and Machine Learning Strategies.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high mortality rate associated with gastric cancer (GC) has resulted in an urgent need to identify novel therapeutic targets for GC. This study aimed to investigate whether GAIP interacting protein, C terminus 1 (GIPC1) represents a therapeutic target and its regulating mechanism in GC. GIPC1 expression was elevated in GC tissues, liver metastasis tissues, and lymph node metastases. GIPC1 knockdown or GIPC1 blocking peptide blocked the platelet-derived growth factor receptor (PDGFR)/PI3K/AKT signaling pathway, and inhibited the proliferation and migration of GC cells. Conversely, GIPC1 overexpression markedly activated the PDGFR/PI3K/AKT signaling pathway, and promoted GC cell proliferation and migration. Furthermore, platelet-derived growth factor subunit BB (PDGF-BB) cytokines and the AKT inhibitor attenuated the effect of differential GIPC1 expression. Moreover, GIPC1 silencing decreased tumor growth and migration in BALB/c nude mice, while GIPC1 overexpression had contrasting effects. Taken together, our findings suggest that GIPC1 functions as an oncogene in GC and plays a central role in regulating cell proliferation and migration via the PDGFR/PI3K/AKT signaling pathway.
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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.