ArticlePloS one2011
Activated K-ras and INK4a/Arf deficiency cooperate during the development of pancreatic cancer by activation of Notch and NF-κB signaling pathways.
Article in PloS one, 2011. 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 It has been retracted, and should not be counted.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 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Contribution of nuclear BCL10 expression to tumor progression and poor prognosis of advanced and/or metastatic pancreatic ductal adenocarcinoma by activating NF-κB-related signaling.Cancer cell international · 2021Article
- Crosstalk between the Notch signaling pathway and non-coding RNAs in gastrointestinal cancers.Oncology letters · 2018Article
- Article
- Genomic characteristics of pancreatic squamous cell carcinoma, an investigation by using high throughput sequencing after in-solution hybrid capture.Oncotarget · 2017Article
- 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
- Niclosamide inhibits colon cancer progression through downregulation of the Notch pathway and upregulation of the tumor suppressor miR-200 family.International journal of molecular medicine · 2016Article
- Loss of Activin Receptor Type 1B Accelerates Development of Intraductal Papillary Mucinous Neoplasms in Mice With Activated KRAS.Gastroenterology · 2016Article
- Genomic expression profiling and bioinformatics analysis of pancreatic cancer.Molecular medicine reports · 2015Article
- Pancreatic cancer stem cells.American journal of cancer research · 2015Review
- Single and Multiple Gene Manipulations in Mouse Models of Human Cancer.Cancer growth and metastasis · 2015Review
- Therapeutic microRNAs targeting the NF-kappa B signaling circuits of cancers.Advanced drug delivery reviews · 2015Review
- Inflammation to cancer: The molecular biology in the pancreas (Review).Oncology letters · 2014Article
- The ZEB1 transcription factor acts in a negative feedback loop with miR200 downstream of Ras and Rb1 to regulate Bmi1 expression.The Journal of biological chemistry · 2014Article
- The Secret Role of microRNAs in Cancer Stem Cell Development and Potential Therapy: A Notch-Pathway Approach.Frontiers in oncology · 2014Review
- Biomarkers for pancreatic cancer: promising new markers and options beyond CA 19-9.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Review
- Friend or foe: emerging role of nuclear factor kappa-light-chain-enhancer of activated B cells in cell senescence.OncoTargets and therapy · 2013Review
- Notch2 inhibits proliferation of chronic myeloid leukemia cells.Oncology letters · 2013Article
- Activated K-Ras and INK4a/Arf deficiency promote aggressiveness of pancreatic cancer by induction of EMT consistent with cancer stem cell phenotype.Journal of cellular physiology · 2013Article
- The role of cancer stem cells and miRNAs in defining the complexities of brain metastasis.Journal of cellular physiology · 2013Review
- Inactivation of Ink4a/Arf leads to deregulated expression of miRNAs in K-Ras transgenic mouse model of pancreatic cancer.Journal of cellular physiology · 2012Article
Corrections and comments
- Retraction · 2018-10-02Falsification/Fabrication of Data · Investigation by Company/Institution · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · Fazlul Sarkar has institutional finding of misconduct;
- Erratum issued
- Retracted
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related death in the United States, suggesting that novel strategies for the prevention and treatment of PDAC are urgently needed. K-ras mutations are observed in >90% of pancreatic cancer, suggesting its role in the initiation and early developmental stages of PDAC. In order to gain mechanistic insight as to the role of mutated K-ras, several mouse models have been developed by targeting a conditionally mutated K-ras(G12D) for recapitulating PDAC. A significant co-operativity has been shown in tumor development and metastasis in a compound mouse model with activated K-ras and Ink4a/Arf deficiency. However, the molecular mechanism(s) by which K-ras and Ink4a/Arf deficiency contribute to PDAC has not been fully elucidated. METHODOLOGY/PRINCIPAL
findingsTo assess the molecular mechanism(s) that are involved in the development of PDAC in the compound transgenic mice with activated K-ras and Ink4a/Arf deficiency, we used multiple methods, such as Real-time RT-PCR, western blotting assay, immunohistochemistry, MTT assay, invasion, EMSA and ELISA. We found that the deletion of Ink4a/Arf in K-ras(G12D) expressing mice leads to PDAC, which is in part mediated through the activation of Notch and NF-κB signaling pathways. Moreover, we found down-regulation of miR-200 family, which could also play important roles in tumor development and progression of PDAC in the compound transgenic mice. CONCLUSIONS/SIGNIFICANCE: Our results suggest that the activation of Notch and NF-κB together with the loss of miR-200 family is mechanistically linked with the development and progression of PDAC in the compound K-ras(G12D) and Ink4a/Arf deficient transgenic mice.
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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.