ArticlePloS one2020
COPB2 gene silencing inhibits colorectal cancer cell proliferation and induces apoptosis via the JNK/c-Jun signaling pathway.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- COPB2 facilitates EDEM3-mediated mannose trimming to sustain ER homeostasis in ovarian cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- The mechanism of Shancigu and its monomer in the development of colorectal cancer based on network pharmacology.Scientific reports · 2025Article
- PSP205, a Novel Phenyl Sulfonyl Piperidine, Induces Apoptotic Cell Death in Colon Cancer by Modulating Coat Protein Complex-Mediated Vesicle Trafficking.ACS pharmacology & translational science · 2025Article
- COPB2 promotes hepatocellular carcinoma progression through regulation of YAP1 nuclear translocation.Oncology research · 2025Article
- Identification of Vesicle-Mediated Transport-Related Genes for Predicting Prognosis, Immunotherapy Response, and Drug Screening in Cervical Cancer.Immunity, inflammation and disease · 2024Article
- SLC12A8 upregulation promotes colorectal cancer progression and chemoresistance.Translational cancer research · 2024Article
- Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.International journal of molecular sciences · 2024Review
- Long noncoding RNA H19: functions and mechanisms in regulating programmed cell death in cancer.Cell death discovery · 2024Review
- A single C-terminal residue controls SARS-CoV-2 spike trafficking and incorporation into VLPs.Nature communications · 2023Article
- Strategies for rapid production of crystallization quality coatomer WD40 domains.Protein expression and purification · 2023Article
- The Impact of YRNAs on HNSCC and HPV Infection.Biomedicines · 2023Article
- Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis.Molecular biology of the cell · 2022Article
- Construction and Validation of an Oxaliplatin-Resistant Gene Signature in Colorectal Cancer Patients Who Underwent Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Comprehensive analysis reveals COPB2 and RYK associated with tumor stages of larynx squamous cell carcinoma.BMC cancer · 2022Article
- Article
- E2F1 Affects the Therapeutic Response to Neoadjuvant Therapy in Breast Cancer.Disease markers · 2022Article
- COPB2: a transport protein with multifaceted roles in cancer development and progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Review
- Molecular Genetics of Microcephaly Primary Hereditary: An Overview.Brain sciences · 2021Review
- An Integrative Pan-Cancer Analysis of the Oncogenic Role of COPB2 in Human Tumors.BioMed research international · 2021Article
- Chrysin Induced Cell Apoptosis ThroughFrontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesColorectal cancer (CRC) is one of the most common malignant human tumors. It is associated with high morbidity and mortality rates. In recent years, tumor gene therapy has emerged as a promising new approach for colorectal cancer therapy. Herein, we identify and analyze the role of COPB2 (coatomer protein complex, subunit beta 2) in proliferation and apoptosis of CRC cells.
methodsTo investigate the role of COPB2 in the proliferation and apoptosis of CRC cells, a shCOPB2 vector and a shCtrl vector were constructed for transfection into RKO and HCT116 cells. Cells proliferation was subsequently measured via cell counting kit-8 (CCK8) assay and Celigo cell counting assay. Apoptosis was measured via flow cytometry. The activity level of Caspase 3/7 was measured. Finally, the level of several JNK/c-Jun apoptosis pathway-related proteins were measured to characterize the mechanism of apoptosis.
resultsOur results showed that the proliferation rate was decreased and the apoptosis rate was increased in shCOPB2-treated RKO and HCT116 cells compared to those in controls. After the silencing of COPB2, JNK/c-Jun signal pathway activation was increased, the expression levels of apoptosis pathway-related proteins, such as Bad, p53 and Caspase 3, were also increased.
conclusionCOPB2 gene silencing can inhibit RKO and HCT116 cells proliferation and induce apoptosis via the JNK/c-Jun signaling pathway.
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