ArticleCancer chemotherapy and pharmacology2021
MiRNA-3662 reverses the gemcitabine resistance in pancreatic cancer through regulating the tumor metabolism.
Article in Cancer chemotherapy and pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- The regulatory roles of non-coding RNAs in aerobic glycolysis and therapeutic potential in pancreatic ductal adenocarcinoma.Annals of medicine · 2026Review
- Molecular Imaging in Pancreatic Cancer: Current Applications and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- MicroRNAs as Biomarkers of Cervical Cancers.International journal of molecular sciences · 2026Review
- Research progress of plant-derived chemical compounds for overcoming pancreatic cancer drug resistance.World journal of gastroenterology · 2026Review
- MicroRNA-based strategies to overcome the immunotherapy barrier in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2026Review
- miR-3662 targets CAB39L to promote proliferation and invasion in gastric cancer.Clinical and experimental medicine · 2025Article
- HypoxamiRs in pancreatic cancer: master regulators of the hypoxic tumor microenvironment.Cell biology and toxicology · 2025Review
- Diagnostic Utility of MicroRNAs in Pancreatic Cancers.Cancers · 2024Review
- Article
- miRNAs in pancreatic cancer progression and metastasis.Clinical & experimental metastasis · 2024Review
- Transitional Insight into the RNA-Based Oligonucleotides in Cancer Treatment.Applied biochemistry and biotechnology · 2024Review
- MicroRNAs: emerging biomarkers and therapeutic targets in pancreatic cancer.Frontiers in molecular biosciences · 2024Review
- microRNAs Associated with Gemcitabine Resistance via EMT, TME, and Drug Metabolism in Pancreatic Cancer.Cancers · 2023Review
- Common Genetic Factors and Pathways in Alzheimer's Disease and Ischemic Stroke: Evidences from GWAS.Genes · 2023Review
- Noncoding RNAs: an emerging modulator of drug resistance in pancreatic cancer.Frontiers in cell and developmental biology · 2023Review
- MicroRNAs and long non-coding RNAs in pancreatic cancer: From epigenetics to potential clinical applications.Translational oncology · 2023Article
- RRP9 promotes gemcitabine resistance in pancreatic cancer via activating AKT signaling pathway.Cell communication and signaling : CCS · 2022Article
- Non-coding RNA in cancer drug resistance: Underlying mechanisms and clinical applications.Frontiers in oncology · 2022Review
- miR-1273h-5p suppresses CXCL12 expression and inhibits gastric cancer cell invasion and metastasis.Open medicine (Warsaw, Poland) · 2022Article
- Glycolysis in the progression of pancreatic cancer.American journal of cancer research · 2022Review
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 2 institutions in 1 country.
Funding
Abstract
objectivesGemcitabine (Gem) is one of the most commonly used chemotherapeutic drugs in treating patients with pancreatic ductal adenocarcinoma (PDAC). Acquired drug resistance against Gem presents a major clinical challenge in the chemotherapy of PDAC. It has been shown that miRNA-3662 is lowly expressed and implicated with quantities of biological processes in cancer. However, whether miRNA-3662 regulates chemoresistance in PDAC remains largely unknown. MATERIALS AND
methodsThe level of miRNA-3662 in PDAC tissues was determined by real-time qPCR (RT-qPCR). Functional experiments were used to investigate the biological role of miRNA-3662 on Gem resistance of PDAC in vitro and in vivo. Fluorescence in situ hybridization (FISH), RT-qPCR, western blotting, bioinformatics analysis and luciferase reporter assay were employed to determine the precise regulation mechanisms.
resultsIn this study, it was investigated that miRNA-3662 was down-regulated in PDAC clinical samples as well as cell lines. Functional assays revealed that miRNA-3662 was sufficient to inhibit Gem resistance in PDAC cells both in vitro and in vivo. Mechanistically, hypoxia-inducible factor 1ɑ (HIF-1ɑ) was one of the transcriptional target of miRNA-3662 and was up-regulated in PDAC samples. Importantly, genetic promoting of HIF-1ɑ largely compromised miR-3662-mediated chemosensitive effects. In addition, miR-3662 could impair the aerobic glycolysis in PDAC cells.
conclusionsThis study sheds light on miRNA-3662 inhibits PDAC cell chemoresistance and aerobic glycolysis through a negative feedback loop with HIF-1ɑ. Therefore, the co-delivery of miR-3662 and Gem could be served as a promising therapeutic regimen for PDAC patients.
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.