ArticleCancer cell international2021
IGHG1 upregulation promoted gastric cancer malignancy via AKT/GSK-3β/β-Catenin pathway.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
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- Proteomic analysis of mouse liver lesions at all three stages of Echinococcus granulosus infection.PLoS neglected tropical diseases · 2024Article
- Immunoglobulin heavy constant gamma 1 silencing decreases tonicity-responsive enhancer-binding protein expression to alleviate diabetic nephropathy.Journal of diabetes investigation · 2024Article
- IGHG1 promotes malignant progression in breast cancer cells through the regulation of AKT and VEGF signaling.Biomolecules & biomedicine · 2023Article
- Integrated analysis of genomic and transcriptomic data for the discovery of splice-associated variants in cancer.Nature communications · 2023Article
- Murine neonatal cardiac B cells promote cardiomyocyte proliferation and heart regeneration.NPJ Regenerative medicine · 2023Article
- Single-cell RNA sequencing reveals tumor immune microenvironment in human hypopharygeal squamous cell carcinoma and lymphatic metastasis.Frontiers in immunology · 2023Article
- Improved profiling of low molecular weight serum proteome for gastric carcinoma by data-independent acquisition.Analytical and bioanalytical chemistry · 2022Article
- Upregulated Expression of Cancer-Derived Immunoglobulin G Is Associated With Progression in Glioma.Frontiers in oncology · 2021Article
- High expression of IGHG1 promotes breast cancer malignant development by activating the AKT pathway.Cell cycle (Georgetown, Tex.)Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite current advances in gastric cancer treatment, disease metastasis and chemo-resistance remain as major hurdles against better overall prognosis. Previous studies indicated that IGHG1 as well as -Catenin serve as important regulators of tumor cellular malignancy. Therefore, understanding detailed molecular mechanism and identifying druggable target will be of great potentials in future therapeutic development.
methodsSurgical tissues and gastric cancer cell lines were retrieved to evaluate IGHG1 expression for patients with or without lymph node/distal organ metastasis. Functional assays including CCK8 assay, Edu assay, sphere formation assay and transwell assay, wound healing assay, etc. were subsequently performed to evaluate the impact of IGHG1/-catenin axis on tumor cell proliferation, migration and chemo-resistance.
resultsGastric cancer tissues and tumor cell lines demonstrated significantly higher level of IGHG1. Functional study further demonstrated that IGHG1 promoted proliferative and migration as well as chemo-resistance of gastric cancer tumor cells. Further experiments indicated that IGHG1 activated AKT/GSK-3/-Catenin axis, which played crucial role in regulation of proliferative and chemo-resistance of gastric cancer cells.
conclusionThis study provided novel evidences that IGHG1 acted as oncogene by promotion of gastric cancer cellular proliferation, migration and chemo-resistance. Our research further suggested that IGHG1/AKT/GSK-3β/β-Catenin axis acted as novel pathway which regulated gastric cancer cellular malignant behavior. Our research might inspire future therapy development to promote overall prognosis of gastric cancer patients.
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