mProX™ Human PHKG1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Cell migration was accelerated by PHKG1 overexpression, and vice versa.
The migration ability of 95D and A549 cells was assessed using a Transwell assay after transfection with PHKG1 siRNA or PHKG1 pcDNA, with statistical significance observed at *p < 0.05, **p < 0.01, and ***p < 0.001 levels. A scale bar of 100 μm was utilized for reference.
Ref: Gu, Jiayi, et al. "Lung adenocarcinoma-derived vWF promotes tumor metastasis by regulating PHKG1-mediated glycogen metabolism." Cancer Science 113.4 (2022): 1362-1376.
Pubmed: 35150045
DOI: 10.1111/cas.15298
Research Highlights
Huang, Xiaolu. et al. "Construction and analysis of expression profile of exosomal lncRNAs in pleural effusion in lung adenocarcinoma." Journal of clinical laboratory analysis, 2022.
The study aimed to identify differentially expressed long-chain non-coding RNA (lncRNAs) and mRNAs in benign and malignant pleural effusion exosomes in order to gain a better understanding of lung adenocarcinoma (LUAD), a highly malignant tumor with a low five-year survival rate. Results showed significant differences in expression levels of lncRNAs and mRNAs between the two types of exosomes, suggesting their potential use as biomarkers for LUAD diagnosis and treatment.
Huang, Xiaolu. et al. "Construction and analysis of expression profile of exosomal lncRNAs in pleural effusion in lung adenocarcinoma." Journal of clinical laboratory analysis, 2022.
Pubmed:
36426920
DOI:
10.1002/jcla.24777
Gu, Jiayi. et al. "Lung adenocarcinoma-derived vWF promotes tumor metastasis by regulating PHKG1-mediated glycogen metabolism." Cancer science, 2022.
In this study, the authors demonstrate that lung adenocarcinoma cells have the ability to produce von Willebrand factor (vWF) and use it to promote tumor metastasis. They also investigate the role of a phosphorylase kinase subunit G1 (PHKG1), a catalytic subtype of phosphorylase kinase (PhK), in this process. Transcriptome sequencing showed that PHKG1 was highly expressed in lung adenocarcinoma patients and correlated with poor prognosis. Further experiments revealed that lung adenocarcinoma-derived vWF regulates PHKG1 expression through the PI3K/AKT pathway, promoting glycogenolysis and funneling glycogen into glycolysis, ultimately resulting in increased tumor metastasis. In vitro and in vivo assays demonstrated that knockdown of PHKG1 or inhibiting phosphorylase activity in combination with vWF overexpression could effectively inhibit metastasis. Overall, the findings suggest that vWF may play a critical role in tumor metastasis by regulating PHKG1 and propose PHKG1 as a potential target for inhibiting lung adenocarcinoma metastasis.
Gu, Jiayi. et al. "Lung adenocarcinoma-derived vWF promotes tumor metastasis by regulating PHKG1-mediated glycogen metabolism." Cancer science, 2022.
Pubmed:
35150045
DOI:
10.1111/cas.15298
