ArticleJournal of Cancer2020
The JAM-B/c-src/MMP9 pathway is associated with progression and regulates the invasion of pancreatic cancer.
Article in Journal of Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Aberrant Expression of JAM2 Inhibits Invasion and Migration in Lung Adenocarcinoma.Cancer reports (Hoboken, N.J.) · 2025Article
- Article
- Transcriptional and Post-Translational Regulation of Junctional Adhesion Molecule-B (JAM-B) in Leukocytes under Inflammatory Stimuli.International journal of molecular sciences · 2022Article
- The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022Review
- PRG2 and AQPEP are misexpressed in fetal membranes in placenta previa and percreta†.Biology of reproduction · 2021Article
- Effects of CXCL12 isoforms in a pancreatic pre-tumour cellular model: Microarray analysis.World journal of gastroenterology · 2021Article
- Interplay between tumor microenvironment and partial EMT as the driver of tumor progression.iScience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Junctional adhesion molecule B (JAM-B) is a multifunctional transmembrane protein that plays an important role in tumor progression. JAM-B is significantly upregulated in gastric cancer, melanoma cell metastasis and oral squamous cell carcinoma. JAM-2 may also function as a putative tumor suppressor in the progression and metastasis of colorectal cancer. The inconsistency of the results in different cancers has led to uncertainty regarding the role of JAM-B in carcinogenesis. For this purpose, the expression levels of JAM-B in pancreatic cancer (PanCa) tissues were associated with T stage and lymph node involvement with significant differences. A relatively high expression of JAM-B was found in PanCa cell lines by immunohistochemistry and western blot analysis. By cell transfection, JAM-B was silenced in tumor cell lines to determine cell invasion and migration abilities. Scratch wound assays and Transwell assays revealed that shJAM-B significantly decreased Panc-1 cell migration and invasion. Experiments were also conducted using a subcutaneous PanCa nude mouse model. A significant difference in tumor diameter at the injection site was found between the control group and the JAM-B low expression group. The expression levels of c-Src and MMP9 were also significantly reduced compared to that in the control group by immunohistochemistry. In conclusion, our results suggest that JAM-B secreted by cancer cells can promote progression and invasion in PanCa by upregulating the c-Src signal and related downstream proteins.
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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.