ArticleBritish journal of cancer2011
Activated KrasG¹²D is associated with invasion and metastasis of pancreatic cancer cells through inhibition of E-cadherin.
Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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55 citing papers in PubMed, 75 citations in OpenAlex.
- ARNTL2 promotes metastatic phenotypes through SERPINE1 transcription in KRAS G12D pancreatic cancer.iScience · 2026Article
- Targeting the DDX3/PAF1 axis enhances chemotherapy efficacy in pancreatic ductal adenocarcinoma.Cancer letters · 2026Article
- Differential effects of KRAS G-domain and hypervariable region mutants on cancer phenotypes.Scientific reports · 2025Article
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- Proactive and reactive roles of TGF-β in cancer.Seminars in cancer biology · 2023Review
- Article
- Inhibiting mutant KRAS G12D gene expression using novel peptide nucleic acid-based antisense: A potential new drug candidate for pancreatic cancer.Oncology letters · 2022Article
- Ubiquitous Aberration in Cholesterol Metabolism across Pancreatic Ductal Adenocarcinoma.Metabolites · 2022Article
- Targeting Mutated KRAS Genes to Treat Solid Tumours.Molecular diagnosis & therapy · 2022Review
- Robust deep learning model for prognostic stratification of pancreatic ductal adenocarcinoma patients.iScience · 2021Article
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- Article
- Acinar transformed ductal cells exhibit differential mucin expression in a tamoxifen-induced pancreatic ductal adenocarcinoma mouse model.Biology open · 2020Article
- CXCR2 signaling promotes secretory cancer-associated fibroblasts in pancreatic ductal adenocarcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Identification of germline and somatic mutations in pancreatic adenosquamous carcinoma using whole exome sequencing.Cancer biomarkers : section A of Disease markers · 2020Article
- Role of ALDH1A1 and HTRA2 expression in CCL2/CCR2-mediated breast cancer cell growth and invasion.Biology open · 2019Article
- Article
- The UCA1/KRAS axis promotes human pancreatic ductal adenocarcinoma stem cell properties and tumor growth.American journal of cancer research · 2019Article
- Axed MUC4 (MUC4/X) aggravates pancreatic malignant phenotype by activating integrin-β1/FAK/ERK pathway.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Generation and testing of clinical-grade exosomes for pancreatic cancer.JCI insight · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPancreatic cancer (PC) harbours an activated point mutation (Kras(G12D)) in the Kras proto-oncogene that has been demonstrated to promote the development of PC.
methodsThis study was designed to investigate the effect of the oncogenic Kras(G12D) allele on aggressiveness and metastatic potential of PC cells. We silenced the oncogenic Kras(G12D) allele expression in CD18/HPAF and ASPC1 cell lines by stable expression of shRNA specific to the Kras(G12D)allele.
resultsThe Kras(G12D) knockdown cells exhibited a significant decrease in motility (P<0.0001), invasion (P<0.0001), anchorage-dependent (P<0.0001) and anchorage-independent growth (P<0.0001), proliferation (P<0.005) and an increase in cell doubling time (P<0.005) in vitro and a decrease in the incidence of metastases upon orthotopic implantation into nude mice. The knockdown of the Kras(G12D) allele led to a significant increase in the expression of E-cadherin (mRNA and protein) both in vitro and in vivo. This was associated with a decrease in the expression of phoshpo-ERK-1/2, NF-κB and MMP-9, and transcription factors such as δEF1, Snail and ETV4. Furthermore, the expression of several proteins involved in cell survival, invasion and metastasis was decreased in the Kras(G12D) knockdown cells.
conclusionsThe results of this study suggest that the Kras(G12D) allele promotes metastasis in PC cells partly through the downregulation of E-cadherin.
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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.