ArticleThe Journal of clinical investigation2023
Pancreatic RECK inactivation promotes cancer formation, epithelial-mesenchymal transition, and metastasis.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 40 citations in OpenAlex.
- The Roles of the Membrane-Anchored Glycoprotein RECK in Animal Development, Tumor Suppression, and Beyond.Life (Basel, Switzerland) · 2026Review
- Unraveling the Predictive Value ofStem cells international · 2026Article
- Cancer-associated fibroblast-derived extracellular vesicles facilitate metastasis in hepatocellular carcinoma by delivering CTGF.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- ASO Therapy Targeting STAU2 to Inhibit Pancreatic Ductal Adenocarcinoma Progression and Metastasis by Regulating the PALLD-Mediated EMT Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MicroRNA‑21: A potential therapeutic target in lung cancer (Review).International journal of oncology · 2025Review
- Effects of SB939 are mediated by STAT3 to inhibit breast cancer cell metastasis-related genes.Oncology letters · 2025Article
- Deciphering the heterogeneity of epithelial cells in pancreatic ductal adenocarcinoma: implications for metastasis and immune evasion.World journal of surgical oncology · 2025Article
- Mechanistic study of quercetin in the treatment of thyroid cancer with diabetes based on network pharmacology andFrontiers in endocrinology · 2025Article
- Exosome applications for the diagnosis and treatment of pancreatic ductal adenocarcinoma: An update (Review).Oncology reports · 2025Review
- The predictive value of Naples prognostic score for patients with locally advanced non-small cell lung cancer undergoing surgery after neoadjuvant chemotherapy.Frontiers in immunology · 2025Article
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- Enhanced expression of miR-20a driven by nanog exacerbated the degradation of extracellular matrix in thoracic aortic dissection.Non-coding RNA research · 2024Article
- Effect of NQO1 Downregulation on the Migration and Invasion of HPV16-Positive Cervical Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Article
- Effect of Emi1 gene silencing on the proliferation and invasion of human breast cancer cells.BMC molecular and cell biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RECK is downregulated in various human cancers; however, how RECK inactivation affects carcinogenesis remains unclear. We addressed this issue in a pancreatic ductal adenocarcinoma (PDAC) mouse model and found that pancreatic Reck deletion dramatically augmented the spontaneous development of PDAC with a mesenchymal phenotype, which was accompanied by increased liver metastases and decreased survival. Lineage tracing revealed that pancreatic Reck deletion induced epithelial-mesenchymal transition (EMT) in PDAC cells, giving rise to inflammatory cancer-associated fibroblast-like cells in mice. Splenic transplantation of Reck-null PDAC cells resulted in numerous liver metastases with a mesenchymal phenotype, whereas reexpression of RECK markedly reduced metastases and changed the PDAC tumor phenotype into an epithelial one. Consistently, low RECK expression correlated with low E-cadherin expression, poor differentiation, metastasis, and poor prognosis in human PDAC. RECK reexpression in the PDAC cells was found to downregulate MMP2 and MMP3, with a concomitant increase in E-cadherin and decrease in EMT-promoting transcription factors. An MMP inhibitor recapitulated the effects of RECK on the expression of E-cadherin and EMT-promoting transcription factors and invasive activity. These results establish the authenticity of RECK as a pancreatic tumor suppressor, provide insights into its underlying mechanisms, and support the idea that RECK could be an important therapeutic effector against human PDAC.
Indexed as
Identifiers
What 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.