ArticleWorld journal of surgical oncology2015
pERK1/2 silencing sensitizes pancreatic cancer BXPC-3 cell to gemcitabine-induced apoptosis via regulating Bax and Bcl-2 expression.
Article in World journal of surgical oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 61 citations in OpenAlex.
- A novel gemcitabine analog as a potential anticancer agent: synthesis andAmerican journal of cancer research · 2025Article
- Different Cytotoxic Effects of Cisplatin on Pancreatic Ductal Adenocarcinoma Cell Lines.International journal of molecular sciences · 2024Article
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- JMJD6-BRD4 complex stimulates lncRNA HOTAIR transcription by binding to the promoter region of HOTAIR and induces radioresistance in liver cancer stem cells.Journal of translational medicine · 2023Article
- Genome, Metabolism, or Immunity: Which Is the Primary Decider of Pancreatic Cancer Fate through Non-Apoptotic Cell Death?Biomedicines · 2023Review
- An 8q24 Gain in Pancreatic Juice Is a Candidate Biomarker for the Detection of Pancreatic Cancer.International journal of molecular sciences · 2023Article
- Pancreatic stellate cell-induced gemcitabine resistance in pancreatic cancer is associated with LDHA- and MCT4-mediated enhanced glycolysis.Cancer cell international · 2023Article
- Emerging Potential Mechanism and Therapeutic Target of Ferroptosis in PDAC: A Promising Future.International journal of molecular sciences · 2022Review
- LINC01207 promotes prostate cancer progression by sponging miR-1182 to upregulate AKT3.Oncology letters · 2022Article
- Attenuation of hepatic ischemia‑reperfusion injury by adipose stem cell‑derived exosome treatment via ERK1/2 and GSK‑3β signaling pathways.International journal of molecular medicine · 2022Article
- The role of metabolic reprogramming in pancreatic cancer chemoresistance.Frontiers in pharmacology · 2022Review
- The Role of Nonapoptotic Programmed Cell Death - Ferroptosis, Necroptosis, and Pyroptosis - in Pancreatic Ductal Adenocarcinoma Treatment.Frontiers in oncology · 2022Review
- Galectin-1-Dependent Mitochondria Apoptosis Plays an Essential Role in the Potential Protein Targets of DBDCT-Induced Hepatotoxicity as Revealed by Quantitative Proteomic Analyses.Bioinorganic chemistry and applications · 2022Article
- Genomic Understanding Reveals the Important Role of FGFR2 as Paeoniflorin Target for Circumventing Breast Cancer Resistance to Tamoxifen.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Antimicrobial peptide 17BIPHE2 inhibits the proliferation of lung cancer cellsOncology letters · 2021Article
- ABCA8-mediated efflux of taurocholic acid contributes to gemcitabine insensitivity in human pancreatic cancer via the S1PR2-ERK pathway.Cell death discovery · 2021Article
- Pancreatic cancer: genetics, disease progression, therapeutic resistance and treatment strategies.Journal of cancer metastasis and treatment · 2021Article
- Mitochondrial Metabolism in PDAC: From Better Knowledge to New Targeting Strategies.Biomedicines · 2020Review
- Anti-Cancer Potential ofMolecules (Basel, Switzerland) · 2020Article
- ZIP4 Increases Expression of Transcription Factor ZEB1 to Promote Integrin α3β1 Signaling and Inhibit Expression of the Gemcitabine Transporter ENT1 in Pancreatic Cancer Cells.Gastroenterology · 2020Article
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Authors and funding
7 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundOur previous study has demonstrated that knockdown of activated ERK1/2(pERK1/2) sensitizes pancreatic cancer cells to chemotherapeutic drug gemcitabine (Gem) treatment. However, the details of this survival mechanism remain undefined. It has also shown that Bcl-2 confers resistance and Bax sensitizes to gemcitabine-induced apoptosis in pancreatic cancer cells. Furthermore, the extracellular signaling-regulated kinase (ERK) signaling pathway regulates Bcl-2/Bax expression ratio. We therefore tested the hypothesis that pancreatic cancer cells are resistant to gemcitabine and this resistance is due to activation of ERK1/2 and subsequent upregulation of Bcl-2 and downregulation of Bax.
methodsPancreatic cancer cell BXPC-3 was used in the study. The effect of pharmacological inhibition of ERK1/2 on resistance of pancreatic cancer cells to apoptosis induced by treatment with gemcitabine was analyzed. The following methods were utilized: TUNEL and ELISA were used to detect apoptosis. Western blot was used to detect the protein expression.
resultsGemcitabine treatment enhanced the activity of ERK1/2 in the BXPC-3 cells. Inhibition of the ERK1/2 by PD98059 could downregulate Bcl-2 and upregulate Bax and was associated with restoration of sensitivity to gemcitabine in BXPC-3 cells. Depletion of endogenous Bcl-2 expression by specific small interfering RNA transfection significantly increased gemcitabine-induced cell apoptosis. Combined treatment with PD98059 and Bax siRNA transfection could decrease gemcitabine-induced ERK1/2 and Bax activation, which subsequently resulted in decreased apoptosis.
conclusionsThe upregulation of ERK1/2-dependent Bcl-2 and downregulation of ERK1/2-dependent Bax can protect human pancreatic cancer cells from gemcitabine-induced apoptosis. Targeting the ERK1/2-Bax/Bcl-2 pathway may in part lead to sensitization of pancreatic cancer to gemcitabine.
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