ArticleThe American journal of pathology2009
HMGA2 maintains oncogenic RAS-induced epithelial-mesenchymal transition in human pancreatic cancer cells.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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
108 citing papers in PubMed, 199 citations in OpenAlex.
- Reexpression of Let-7g microRNA inhibits the proliferation and migration via K-Ras/HMGA2/snail axis in hepatocellular carcinoma.BioMed research international · 2014Trial
- High-throughput drug screening identifies EGFR/MAPK pathway targeting sensitivities in organoid models of ovarian carcinosarcoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Unveiling Let-7a's Therapeutic Role in Ewing Sarcoma Through Molecular Docking and Deformation Energy Analysis.Current issues in molecular biology · 2025Article
- Prognostic model identification of ribosome biogenesis-related genes in pancreatic cancer based on multiple machine learning analyses.Discover oncology · 2025Article
- HMGA2 Expression Predicts Subtype, Survival, and Treatment Outcome in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- HMGA2 Overexpression in Papillary Thyroid Cancer Promotes Thyroid Cell Dedifferentiation and Invasion, and These Effects Are Counteracted by Suramin.International journal of molecular sciences · 2025Article
- Menin in Cancer.Genes · 2024Review
- Decoding high mobility group A2 protein expression regulation and implications in human cancers.Discover oncology · 2024Review
- HMGA2 promotes resistance against paclitaxel by targeting the p53 signaling pathway in colorectal cancer cells.Heliyon · 2024Article
- HMGA2 alleviates ferroptosis by promoting GPX4 expression in pancreatic cancer cells.Cell death & disease · 2024Article
- Diverse activity of miR-150 in Tumor development: shedding light on the potential mechanisms.Cancer cell international · 2023Review
- Significance of High-Mobility Group A Protein 2 Expression in Pancreatic Ductal Adenocarcinoma and Ampullary Adenocarcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- Differential expression and bioinformatics analysis of exosome circRNAs in pancreatic ductal adenocarcinoma.Translational oncology · 2023Article
- Unraveling the Roles of miR-204-5p and HMGA2 in Papillary Thyroid Cancer Tumorigenesis.International journal of molecular sciences · 2023Article
- miR-219-5p attenuates cisplatin resistance of ovarian cancer by inactivating Wnt/β-catenin signaling and autophagy via targeting HMGA2.Cancer gene therapy · 2023Article
- The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis.Journal of hematology & oncology · 2022Review
- Expression and Clinical Significance of High-Mobility Group AT-hook 2 (HMGA2) in Osteosarcoma.Orthopaedic surgery · 2022Article
- Circular RNA circZFR Promotes Hepatocellular Carcinoma Progression by Regulating miR-375/HMGA2 Axis.Digestive diseases and sciences · 2021Article
- Prognostic significance of high mobility group A2 (HMGA2) in pancreatic ductal adenocarcinoma: malignant functions of cytoplasmic HMGA2 expression.Journal of cancer research and clinical oncology · 2021Article
- Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer is a highly aggressive malignancy due to elevated mitotic activities and epithelial-mesenchymal transition (EMT). Oncogenic RAS and transforming growth factor-beta signaling are implicated in these malignant features. The mechanisms that underlie EMT need to be addressed since it promotes tissue invasion and metastasis. The high-mobility group A protein 2 (HMGA2) is a non-histone chromatin factor that is primarily expressed in undifferentiated tissues and tumors of mesenchymal origin. However, its role in EMT in pancreatic cancer is largely unknown. Here we report that HMGA2 is involved in EMT maintenance in human pancreatic cancer cells. Specific knockdown of HMGA2 inhibited cell proliferation, leading to an epithelial-state transition that restores cell-cell contact due to E-cadherin up-regulation. Consistently, an inverse correlation between HMGA2-positive cells and E-cadherin-positive cells was found in cancer tissues. Inhibition of the RAS/MEK pathway also induced an epithelial transition, together with HMGA2 down-regulation. Transcriptional repressors of the E-cadherin gene, such as SNAIL, decreased after HMGA2 knockdown since HMGA2 directly activated the SNAlL gene promoter. The decrease of SNAIL after RAS/MEK inhibition was suppressed by HMGA2 overexpression. Further, let-7 microRNA-mediated HMGA2 down-regulation had no effect on the prevention of the transformed phenotype in these cells. These data shed light on the importance of HMGA2 in reversibly maintaining EMT, suggesting that HMGA2 is a potential therapeutic target for the treatment of pancreatic cancer.
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.