ArticlePloS one2014
Cooperativity of oncogenic K-ras and downregulated p16/INK4A in human pancreatic tumorigenesis.
Article in PloS one, 2014. 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 It has been retracted, and should not be counted.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 33 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
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Pathogenic KRAS variants disrupt structure and dynamics: Insights from integrated computational analyses.PloS one · 2026Article
- Senescence program and its reprogramming in pancreatic premalignancy.Cell death & disease · 2023Review
- Cell-Autonomous Cxcl1 Sustains Tolerogenic Circuitries and Stromal Inflammation via Neutrophil-Derived TNF in Pancreatic Cancer.Cancer discovery · 2023Article
- Mutant KRAS drives metabolic reprogramming and autophagic flux in premalignant pancreatic cells.Cancer gene therapy · 2022Article
- CES2 sustains HNF4α expression to promote pancreatic adenocarcinoma progression through an epoxide hydrolase-dependent regulatory loop.Molecular metabolism · 2022Article
- KRAS is a prognostic biomarker associated with diagnosis and treatment in multiple cancers.Frontiers in genetics · 2022Article
- Combined Blockade of MEK and CDK4/6 Pathways Induces Senescence to Improve Survival in Pancreatic Ductal Adenocarcinoma.Molecular cancer therapeutics · 2021Article
- BCL6 confers KRAS-mutant non-small-cell lung cancer resistance to BET inhibitors.The Journal of clinical investigation · 2021Article
- Comprehensive Analysis Revealed thatFrontiers in cell and developmental biology · 2021Article
- Interleukin-1 receptor antagonist enhances chemosensitivity to fluorouracil in treatment of Kras mutant colon cancer.World journal of gastrointestinal oncology · 2020Article
- Clinical significance of SQSTM1/P62 and nuclear factor-κB expression in pancreatic carcinoma.World journal of gastrointestinal oncology · 2020Article
- The overexpression of long intergenic ncRNA00162 induced by RelA/p65 promotes growth of pancreatic ductal adenocarcinoma.Cell proliferation · 2020Article
- Suppression of the SLC7A11/glutathione axis causes synthetic lethality in KRAS-mutant lung adenocarcinoma.The Journal of clinical investigation · 2020Article
- Targeting retinoblastoma protein phosphorylation in combination with EGFR inhibition in pancreatic cancer cells.International journal of oncology · 2019Article
- Expression of Concern: Cooperativity of Oncogenic K-Ras and Downregulated p16/INK4A in Human Pancreatic Tumorigenesis.PloS one · 2019Article
- Therapeutic strategies to target RAS-mutant cancers.Nature reviews. Clinical oncology · 2018Review
- p16, p21, and p53 proteins play an important role in development of pancreatic intraepithelial neoplastic.Irish journal of medical science · 2018Article
- dNTP metabolism links mechanical cues and YAP/TAZ to cell growth and oncogene-induced senescence.The EMBO journal · 2018Article
- Inhibition of enhancer of zeste homolog 2 increases the expression of p16 and suppresses the proliferation and migration of ovarian carcinoma cellsOncology letters · 2018Article
- SOX9 activity is induced by oncogenic Kras to affect MDC1 and MCMs expression in pancreatic cancer.Oncogene · 2018Article
Corrections and comments
- Expression of concern · 2019-11-08Concerns/Issues about Data · Concerns/Issues about Image ·
- Expression of concern
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Activation of K-ras and inactivation of p16 are the most frequently identified genetic alterations in human pancreatic epithelial adenocarcinoma (PDAC). Mouse models engineered with mutant K-ras and deleted p16 recapitulate key pathological features of PDAC. However, a human cell culture transformation model that recapitulates the human pancreatic molecular carcinogenesis is lacking. In this study, we investigated the role of p16 in hTERT-immortalized human pancreatic epithelial nestin-expressing (HPNE) cells expressing mutant K-ras (K-rasG12V). We found that expression of p16 was induced by oncogenic K-ras in these HPNE cells and that silencing of this induced p16 expression resulted in tumorigenic transformation and development of metastatic PDAC in an orthotopic xenograft mouse model. Our results revealed that PI3K/Akt, ERK1/2 pathways and TGFα signaling were activated by K-ras and involved in the malignant transformation of human pancreatic cells. Also, p38/MAPK pathway was involved in p16 up-regulation. Thus, our findings establish an experimental cell-based model for dissecting signaling pathways in the development of human PDAC. This model provides an important tool for studying the molecular basis of PDAC development and gaining insight into signaling mechanisms and potential new therapeutic targets for altered oncogenic signaling pathways in PDAC.
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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.