ArticleOncology letters2018
Conversion of epithelial-to-mesenchymal transition to mesenchymal-to-epithelial transition is mediated by oxygen concentration in pancreatic cancer cells.
Article in Oncology letters, 2018. 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 It has been retracted, and should not be counted.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 20 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
20 citing papers in PubMed.
- Cyclooxygenases in pancreatic ductal adenocarcinoma: are they inflammatory catalysts for tumor growth.Frontiers in oncology · 2026Review
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- Colony‑stimulating factor CSF2 mediates the phenotypic plasticity of small‑cell lung cancer by regulating the p‑STAT3/MYC pathway.Oncology reports · 2022Article
- The Role ofCancers · 2022Review
- DNA Methylation Mediates EMT Gene Expression in Human Pancreatic Ductal Adenocarcinoma Cell Lines.International journal of molecular sciences · 2022Article
- Epithelial to Mesenchymal Transition: A Challenging Playground for Translational Research. Current Models and Focus onInternational journal of molecular sciences · 2021Review
- Review
- Review
- Epithelial-to-Mesenchymal Transition in the Light of Plasticity and Hybrid E/M States.Journal of clinical medicine · 2021Review
- Interplay between tumor microenvironment and partial EMT as the driver of tumor progression.iScience · 2021Review
- Targeting hypoxic tumor microenvironment in pancreatic cancer.Journal of hematology & oncology · 2021Review
- Hypoxia, partial EMT and collective migration: Emerging culprits in metastasis.Translational oncology · 2020Review
- Lineage plasticity in cancer: a shared pathway of therapeutic resistance.Nature reviews. Clinical oncology · 2020Review
- Adapt and conquer: Metabolic flexibility in cancer growth, invasion and evasion.Molecular metabolism · 2020Review
- Insulin-producing organoids engineered from islet and amniotic epithelial cells to treat diabetes.Nature communications · 2019Article
- Colorectal metastasis to the gallbladder mimicking a primary gallbladder malignancy: histopathological and molecular characteristics.Histopathology · 2019Article
- Tumor-stromal crosstalk in pancreatic cancer and tissue fibrosis.Molecular cancer · 2019Review
- Establishment of primary human breast cancer cell lines using "pulsed hypoxia" method and development of metastatic tumor model in immunodeficient mice.Cancer cell international · 2019Article
- Eco-evolutionary causes and consequences of temporal changes in intratumoural blood flow.Nature reviews. Cancer · 2018Review
- Epithelial-Mesenchymal Transition: Role in Cancer Progression and the Perspectives of Antitumor Treatment.Acta naturaeArticle
Corrections and comments
- Retraction · 2022-02-04Concerns/Issues about Data · Concerns/Issues about Image · Objections by Third Party · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor metastasis is accompanied by a two-stage process of epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET). Currently, the exact mechanisms underlying EMT-MET conversion are unclear. In the present study, the mechanisms by which primary sites (hypoxic) and homing sites (normoxic or hyperoxic) participate in EMT-MET conversion were evaluated. Pancreatic cancer cells were grown under different oxygenation conditions. Cell morphology and epithelial (E)-cadherin and vimentin expression were examined. Transwell chambers were used to examine tumor invasiveness, and scratch assays were performed to examine cell migration. Reverse transcription-polymerase chain reaction and western blot analysis were used to quantitate the mRNA and protein expression of E-cadherin, vimentin, Snail and hypoxia-inducible factor (HIF)-1α. BxPc-3 and Panc-1 cells grown under hypoxic conditions demonstrated increased partial EMT, reduced E-cadherin expression, and increased vimentin expression, compared with cells grown under normoxic or hyperoxic conditions. Cells grown under hypoxic conditions also indicated increased migration and invasiveness. HIF-1α mRNA and protein expression was increased in cells grown under hypoxic conditions. These changes were reversed when a specific inhibitor of the HIF-1α receptor was used to block HIF-1α signaling. Differences in oxygen concentration at primary sites and homing sites are important in the EMT-MET process, and the underlying mechanism may involve HIF-1α-Snail signaling.
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.