ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
miR-33a suppresses the nuclear translocation of β-catenin to enhance gemcitabine sensitivity in human pancreatic cancer cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Abnormal levels of miRNA in pancreatic cancer are linked to tumor progression by regulating the translation of tumor-associated mRNA.Annals of medicine · 2025Review
- β-catenin inhibitors in cancer therapeutics: intricacies and way forward.Bioengineered · 2023Review
- Nanoparticle-Mediated Therapy with miR-198 Sensitizes Pancreatic Cancer to Gemcitabine Treatment through Downregulation of VCP-Mediated Autophagy.Pharmaceutics · 2023Article
- Article
- Noncoding RNAs: an emerging modulator of drug resistance in pancreatic cancer.Frontiers in cell and developmental biology · 2023Review
- Epithelial to Mesenchymal Transition as Mechanism of Progression of Pancreatic Cancer: From Mice to Men.Cancers · 2022Review
- Predictive Biomarkers for a Personalized Approach in Resectable Pancreatic Cancer.Frontiers in surgery · 2022Review
- Recent Advances in Pancreatic Cancer: Novel Prognostic Biomarkers and Targeted Therapy-A Review of the Literature.Biomolecules · 2021Review
- Context Matters-Why We Need to Change From a One Size Fits all Approach to Made-to-Measure Therapies for Individual Patients With Pancreatic Cancer.Frontiers in cell and developmental biology · 2021Review
- Teaching an old dog new tricks: reactivated developmental signaling pathways regulate ABCB1 and chemoresistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- MicroRNAs target the Wnt/β‑catenin signaling pathway to regulate epithelial‑mesenchymal transition in cancer (Review).Oncology reports · 2020Review
- Role of microRNA-33a in malignant cells.Oncology letters · 2020Review
- AREG mediates the epithelial‑mesenchymal transition in pancreatic cancer cells via the EGFR/ERK/NF‑κB signalling pathway.Oncology reports · 2020Article
- MicroRNAs in Pancreatic Cancer: biomarkers, prognostic, and therapeutic modulators.BMC cancer · 2019Review
- Wnt/β-Catenin Signaling: The Culprit in Pancreatic Carcinogenesis and Therapeutic Resistance.International journal of molecular sciences · 2019Review
- Downregulation of miR-183 inhibits the growth of PANC-1 pancreatic cancer cellsExperimental and therapeutic medicine · 2019Article
- Article
- The Network of Non-coding RNAs in Cancer Drug Resistance.Frontiers in oncology · 2018Review
- MicroRNA-410-3p attenuates gemcitabine resistance in pancreatic ductal adenocarcinoma by inhibiting HMGB1-mediated autophagy.Oncotarget · 2017Article
- Biological function and mechanism of miR-33a in prostate cancer survival and metastasis: via downregulating Engrailed-2.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, partly due to its high level of drug resistance. β-Catenin is critical for drug resistance in pancreatic cancer, which occurs through multiple mechanisms. Here, we observed that miR-33a targeted the 3'UTR of β-catenin, inducing apoptosis and inhibiting the growth of human pancreatic cancer cells. Moreover, gemcitabine (GEM) treatment enhanced β-catenin expression by reducing miR-33a expression in a dose-dependent manner. GEM-resistant MiaPaCa-2(res) cells with a low level of miR-33a expression and high level of β-catenin expression adopted spindle-shaped morphologies, similar to their morphologies during the epithelial-to-mesenchymal transition (EMT), and their normal morphologies were restored by miR-33a overexpression. Furthermore, miR-33a downregulated β-catenin nuclear translocation, decreasing the transcription of survivin, cyclin D1, and MDR-1, and the protein expression of slug, vimentin, and N-cadherin, thereby mediating sensitization to GEM. Thus, miR-33a might function as a tumor suppressor to downregulate β-catenin expression, affecting cell growth, apoptosis, the EMT, and GEM resistance.
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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.