ArticleJournal of cellular physiology2013
Activated K-Ras and INK4a/Arf deficiency promote aggressiveness of pancreatic cancer by induction of EMT consistent with cancer stem cell phenotype.
Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6/JAK2/STAT3 Axis in Pancreatic Cancer.Cancer medicine · 2025Article
- Exosome applications for the diagnosis and treatment of pancreatic ductal adenocarcinoma: An update (Review).Oncology reports · 2025Review
- Epithelial-mesenchymal transition: a hallmark in pancreatic cancer stem cell migration, metastasis formation, and drug resistance.Journal of cancer metastasis and treatment · 2020Article
- Novel compound cedrelone inhibits hepatocellular carcinoma progression via PBLD and Ras/Rap1.Experimental and therapeutic medicine · 2019Article
- Palladium based nanoparticles for the treatment of advanced melanoma.Scientific reports · 2019Article
- Platelet-derived growth factor-D promotes colorectal cancer cell migration, invasion and proliferation by regulating Notch1 and matrix metalloproteinase-9.Oncology letters · 2018Article
- Effect of Bmi-1-mediated NF-κB signaling pathway on the stem-like properties of CD133+ human liver cancer cells.Cancer biomarkers : section A of Disease markers · 2018Article
- Methyl-CpG-binding domain 3 inhibits epithelial-mesenchymal transition in pancreatic cancer cells via TGF-β/Smad signalling.British journal of cancer · 2017Article
- MET: roles in epithelial-mesenchymal transition and cancer stemness.Annals of translational medicine · 2017Review
- Therapeutic potential of GW501516 and the role of Peroxisome proliferator-activated receptor β/δ and B-cell lymphoma 6 in inflammatory signaling in human pancreatic cancer cells.Biochemistry and biophysics reports · 2016Article
- Suppression of MicroRNA 200 Family Expression by Oncogenic KRAS Activation Promotes Cell Survival and Epithelial-Mesenchymal Transition in KRAS-Driven Cancer.Molecular and cellular biology · 2016Article
- Retraction: "Activated K-Ras and INK4a/Arf Deficiency Promote Aggressiveness of Pancreatic Cancer by Induction of EMT Consistent With Cancer Stem Cell Phenotype" by Wang et al.Journal of cellular physiology · 2016Article
- TAp73 loss favors Smad-independent TGF-β signaling that drives EMT in pancreatic ductal adenocarcinoma.Cell death and differentiation · 2016Article
- Article
- Pancreatic cancer stem cell markers and exosomes - the incentive push.World journal of gastroenterology · 2016Review
- Clinical significance of platelet derived growth factor-C and -D in gastric cancer.Oncology letters · 2015Article
- Human papillomavirus 16 (HPV16) enhances tumor growth and cancer stemness of HPV-negative oral/oropharyngeal squamous cell carcinoma cells via miR-181 regulation.Papillomavirus research (Amsterdam, Netherlands) · 2015Article
- Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer.Nature · 2015Article
- Up-regulation of UHRF1 by oncogenic Ras promoted the growth, migration, and metastasis of pancreatic cancer cells.Molecular and cellular biochemistry · 2015Article
- Mining for Candidate Genes Related to Pancreatic Cancer Using Protein-Protein Interactions and a Shortest Path Approach.BioMed research international · 2015Article
Corrections and comments
- Correction · 2014-04-23Error in Image · Updated to Retraction · · Wayne State University investigated Fazlul Sarkar
- Retraction · 2016-06-17Duplication of/in Image · Investigation by Company/Institution · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Upgrade/Update of Prior Notice(s) · · Wayne State University investigated Fazlul Sarkar
- Erratum issued
- Retracted
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most frequently diagnosed cancers and the fourth leading cause of cancer-related death in the United States, suggesting that there is an urgent need to design novel strategies for achieving better treatment outcome of patients diagnosed with PDAC. Our previous study has shown that activation of Notch and NF-κB play a critical role in the development of PDAC in the compound K-Ras(G12D) and Ink4a/Arf deficient transgenic mice. However, the exact molecular mechanism by which mutated K-Ras and Ink4a/Arf deficiency contribute to progression of PDAC remains largely elusive. In the present study, we used multiple methods, such as real-time RT-PCR, Western blotting assay, and immunohistochemistry to gain further mechanistic insight. We found that the deletion of Ink4a/Arf in K-Ras(G12D) expressing mice led to high expression of PDGF-D signaling pathway in the tumor and tumor-derived cell line (RInk-1 cells). Furthermore, PDGF-D knock-down in RInk-1 cells resulted in the inhibition of pancreatosphere formation and down-regulation of EZH2, CD44, EpCAM, and vimentin. Moreover, we demonstrated that epithelial-mesenchymal transition (EMT) was induced in the compound mice, which is linked with aggressiveness of PDAC. In addition, we demonstrated that tumors from compound transgenic mice have higher expression of cancer stem cell (CSC) markers. These results suggest that the acquisition of EMT phenotype and induction of CSC characteristics could be linked with the aggressiveness of PDAC mediated in part through the activation of PDGF-D, signaling.
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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.