ArticleAging2021
Praja2 suppresses the growth of gastric cancer by ubiquitylation of KSR1 and inhibiting MEK-ERK signal pathways.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- ERCC6L drives lung adenocarcinoma metastasis: a PJA2/p53 ubiquitination-dependent mechanism.Respiratory research · 2026Article
- Transcriptome-Wide Cox Regression Identifies Candidate Survival-Associated Genes in Newly Diagnosed Acute Myeloid Leukemia.Cancer informatics · 2026Article
- Aberrant PJA2-CHRM3 signaling creates a therapeutic vulnerability in gastric tumor.British journal of cancer · 2025Article
- CENPs in hepatocellular carcinoma: a comprehensive review of expression patterns, clinical correlations, and functional mechanisms.American journal of cancer research · 2025Review
- ZC3H13 promotes autophagy in bladder cancer through m6A methylation modification of PJA2 and ubiquitination of KSR1.Human cell · 2024Article
- The relationship and clinical significance of lactylation modification in digestive system tumors.Cancer cell international · 2024Review
- Downregulation of praja2 restrains endocytosis and boosts tyrosine kinase receptors in kidney cancer.Communications biology · 2024Article
- UPS: Opportunities and challenges for gastric cancer treatment.Frontiers in oncology · 2023Review
- Targeted inhibition of ubiquitin signaling reverses metabolic reprogramming and suppresses glioblastoma growth.Communications biology · 2022Article
- Interactome Analysis of Human Phospholipase D and Phosphatidic Acid-Associated Protein Network.Molecular & cellular proteomics : MCP · 2022Article
- Bevacizumab-Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is a common malignant tumor, which has a high incidence and fatality. Therefore, it is important to clarify the molecular mechanism of the occurrence and development for GC and to find more effective treatments and targeted drugs. In this study, we found that the kinase suppressor of Ras1 (KSR1) was increased in GC tissues and cell lines. Silencing of KSR1 inhibited the proliferation, migration and invasion of MKN-45 cells. E3 ligase Praja2 was downregulated in GC tissues and cell lines. In addition, praja2 promoted ubiquitylation of KSR1, but inhibited MEK-ERK signal pathways. Functional analysis indicated overexpression of praja2 inhibited the proliferation, migration and invasion of MKN-45 cells, while MG132 or FGF2 treatment removed the inhibitory effects of praja2 on GC progression.
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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.