ArticleMolecular oncology2017
Loss of AMPK activation promotes the invasion and metastasis of pancreatic cancer through an HSF1-dependent pathway.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Exploring the logic and conducting a comprehensive evaluation of AdipoRon-based adiponectin replacement therapy against hormone-related cancers-a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Pooled it
- Exploring the Interplay Between Hyperthermia and Cytotoxic Drugs in Ocular Melanoma Cell Lines: Implications and Variability in Treatment Efficiency.Investigative ophthalmology & visual science · 2025Article
- Article
- Knockdown of HSF1 inhibits invasion, metastasis, and proliferation of endometrial carcinoma cells while promoting apoptosis.Cancer biomarkers : section A of Disease markers · 2025Article
- The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Review
- A Novel AMPK Inhibitor Sensitizes Pancreatic Cancer Cells to Ferroptosis Induction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- New Function Annotation of PROSER2 in Pancreatic Ductal Adenocarcinoma.Journal of proteome research · 2024Article
- The Molecular Twin artificial-intelligence platform integrates multi-omic data to predict outcomes for pancreatic adenocarcinoma patients.Nature cancer · 2024Article
- HSF1 at the crossroads of chemoresistance: from current insights to future horizons in cell death mechanisms.Frontiers in cell and developmental biology · 2024Review
- The small-molecule drug homoharringtonine targets HSF1 to suppress pancreatic cancer progression.American journal of cancer research · 2024Article
- Targeted Inhibition of Hsp90 in Combination with Metformin Modulates Programmed Cell Death Pathways in A549 Lung Cancer Cells.Applied biochemistry and biotechnology · 2023Article
- An Increase in HSF1 Expression Directs Human Mammary Epithelial Cells toward a Mesenchymal Phenotype.Cancers · 2023Article
- Molecular and metabolic regulation of immunosuppression in metastatic pancreatic ductal adenocarcinoma.Molecular cancer · 2023Review
- Impact of AMPK on cervical carcinoma progression and metastasis.Cell death & disease · 2023Article
- HSF1, Aging, and Neurodegeneration.Advances in experimental medicine and biology · 2023Review
- AMPK promotes Arf6 activation in a kinase-independent manner upon glucose starvation.Journal of cell science · 2022Article
- Therapeutic Intervention in Cancer by Isoliquiritigenin from Licorice: A Natural Antioxidant and Redox Regulator.Antioxidants (Basel, Switzerland) · 2022Review
- Metformin Enhances TKI-Afatinib Cytotoxic Effect, Causing Downregulation of Glycolysis, Epithelial-Mesenchymal Transition, and EGFR-Signaling Pathway Activation in Lung Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Neuroprotective Effect of IND1316, an Indole-Based AMPK Activator, in Animal Models of Huntington Disease.ACS chemical neuroscience · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with a mortality rate that closely parallels its incidence rate, and a better understanding of the molecular and cellular mechanisms associated with the invasion and distant metastasis is required. Heat shock factor 1 (HSF1) is a very highly conserved factor in eukaryotes that regulates the protective heat shock response. Here, we show that HSF1 is abnormally activated in pancreatic cancer. The knockdown of HSF1 impaired the invasion and migration and epithelial-mesenchymal transition (EMT) of pancreatic cancer cells in vitro; however, the upregulation of HSF1 showed the opposite effects. In vivo, the pharmacological inhibition of HSF1 significantly reduced the tumor burden, decreased the incidence of invasion, and prolonged the overall survival of transgenic mice harboring the spontaneous pancreatic cancer. We suggest that the loss of AMP-activated protein kinase (AMPK) activation mediates the abnormal activation of HSF1 based on the findings that phospho-HSF1 (p-HSF1) was highly expressed in human PDAC tissues with a low expression of p-AMPK and that in those tissues with a high p-AMPK expression, the level of p-HSF1 was decreased. The in vivo and in vitro activation of AMPK impaired the activity of HSF1, and HSF1 mediated the effects of the AMPK knockdown-induced pancreatic cancer invasion and migration. Our study revealed a novel mechanism by which the loss of AMPK activation amplifies the activity of HSF1 to promote the invasion and metastasis of pancreatic cancer.
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