ArticleAmerican journal of translational research2020
Tetraspanin CD9 interacts with α-secretase to enhance its oncogenic function in pancreatic cancer.
Article in American journal of translational research, 2020. 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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Who cites it
10 citing papers in PubMed.
- CircRNA hsa_circ_0004781 promoted cell proliferation by acting as a sponge for miR-9-5p and miR-338-3p and upregulating KLF5 and ADAM17 expression in pancreatic ductal adenocarcinoma.Cancer cell international · 2025Article
- Regulation of ADAM10 activity through microdomain-dependent intracellular calcium changes.Cell communication and signaling : CCS · 2024Article
- Secretase promotes AD progression: simultaneously cleave Notch and APP.Frontiers in aging neuroscience · 2024Review
- The role of Tetraspanins in digestive system tumor development: update and emerging evidence.Frontiers in cell and developmental biology · 2024Review
- Prognostic value and multifaceted roles of tetraspanin CD9 in cancer.Frontiers in oncology · 2023Review
- Tissue Biomarkers Predicting Lymph Node Status in Cutaneous Melanoma.International journal of molecular sciences · 2022Review
- ALCAM: A Novel Surface Marker on EpCAMBiomedicines · 2022Article
- Neoadjuvant chemotherapy endows CD9 with prognostic value that differs between tumor and stromal areas in patients with pancreatic cancer.Journal of clinical laboratory analysis · 2022Article
- Tetraspanin CD9 Expression Predicts Sentinel Node Status in Patients with Cutaneous Melanoma.International journal of molecular sciences · 2022Article
- Recent Advances in the Delivery Carriers and Chemical Conjugation Strategies for Nucleic Acid Drugs.Cancers · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer is one of the most lethal cancers and its prognosis remains poor. ADAM family proteins like ADAM10, ADAM9 and ADAM17 function as α-secretase to cleavage cell surface proteins like Notch to facilitate oncogenesis in various tumors. The oncogenic roles of α-secretase in PDAC have been demonstrated but it remains unknown that whether and how α-secretase is regulated in PDAC. Here, we report that the expression of tetraspanin CD9 was increased and strongly associated with poor prognosis in PDAC. CD9 expression was positively associated with α-secretase activity in PDAC tissues and CD9 knock-down inhibited α-secretase activity in PDAC cell lines. Co-immunoprecipitation and GST pull down demonstrates that CD9 directly interacted with ADAM10, ADAM9 and ADAM17, respectively. Cell surface biotin labeling and immunostaining of tagged ADAM proteins show that CD9 promoted cell surface trafficking of ADAM family proteins. In addition, the antibody targeting extracellular domain of CD9 disrupted the interactions between CD9 and ADAM family proteins, reduced cell surface trafficking of ADAM proteins and inhibited α-secretase activity. Notch signaling was inhibited by CD9 knockdown or CD9 antibody in cell lines. Finally, CD9 antibody showed anti-tumor effects in cell proliferation MTT assay, transwell migration assay and colony formation assay. Our study reveals a novel CD9/ADAM/Notch signaling network in PDAC and it supports that targeting CD9-ADAM interaction with antibody may be a potential therapeutic intervention for PDAC.
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Identifiers
33042435PMC7540085What OpenQuestion holds
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.