ArticleScientific reports2016
MIA PaCa-2 and PANC-1 - pancreas ductal adenocarcinoma cell lines with neuroendocrine differentiation and somatostatin receptors.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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111 citing papers in PubMed, 169 citations in OpenAlex.
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- MSC-derived exosomes co-delivering anti-miR-221 and gemcitabine for inhibiting the proliferation of pancreatic cancer.Journal of translational medicine · 2026Article
- From Oncolysis to Adaptive Immunity: Yellow Fever Virus 17D and Ruxolitinib Activate Antitumor Immune Responses in Pancreatic Cancer Models.Biomedicines · 2026Article
- LncRNA YIYA drives pancreatic cancer proliferation under high-glucose conditions by reinforcing a RAS-PKM2-dependent Warburg phenotype.FEBS letters · 2026Article
- The anticancer effects of PCAIs in pancreatic cancer cells involve MAPK and PI3K/AKT pathways hyperactivation.Oncotarget · 2026Article
- A Novel Microfluidic System for Immunomagnetic Isolation of Pancreatic Cancer CTCs: Plectin‑1 and EpCAM as Potential Tumor Markers.ACS omega · 2026Article
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- Comparative Proteomic Profiling of Responses to Standard Systemic Treatment Regimens in Pancreatic Cancer.Cells · 2026Article
- Vitamin D Protects Pancreatic Cancer (PC) Cells from Death and DNA Damage Induced by Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Article
- A type of pancreatic cancer cells form cell clusters from a solitary condition in a primary ciliogenesis-dependent manner.Medical molecular morphology · 2025Article
- Assessment of Tumor Relative Biological Effectiveness in Low-LET Proton Irradiation.Biomedicines · 2025Article
- A base editing platform for the correction of cancer driver mutations unmasks conserved p53 transcription programs.Genome biology · 2025Article
- eEF2K is a poor prognostic factor and novel molecular target in pancreatic cancer: regulating tumor growth and progression via the tumor microenvironment.Cell death & disease · 2025Article
- Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure-Based Virtual Screening.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- uPAR Immuno-PET in Pancreatic Cancer, Aging, and Chemotherapy-Induced Senescence.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024Article
- The Role of Heat Shock Factor 1 in Preserving Proteomic Integrity During Copper-Induced Cellular Toxicity.International journal of molecular sciences · 2024Article
51 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies using cell lines should always characterize these cells to ensure that the results are not distorted by unexpected morphological or genetic changes possibly due to culture time or passage number. Thus, the aim of this study was to describe those MIA PaCa-2 and PANC-1 cell line phenotype and genotype characteristics that may play a crucial role in pancreatic cancer therapeutic assays, namely neuroendocrine chemotherapy and peptide receptor radionuclide therapy. Epithelial, mesenchymal, endocrine and stem cell marker characterization was performed by immunohistochemistry and flow cytometry, and genotyping by PCR, gene sequencing and capillary electrophoresis. MIA PaCa-2 (polymorphism) expresses CK5.6, AE1/AE3, E-cadherin, vimentin, chromogranin A, synaptophysin, SSTR2 and NTR1 but not CD56. PANC-1 (pleomorphism) expresses CK5.6, MNF-116, vimentin, chromogranin A, CD56 and SSTR2 but not E-cadherin, synaptophysin or NTR1. MIA PaCA-1 is CD24(-), CD44(+/++), CD326(-/+) and CD133/1(-), while PANC-1 is CD24(-/+), CD44(+), CD326(-/+) and CD133/1(-). Both cell lines have KRAS and TP53 mutations and homozygous deletions including the first 3 exons of CDKN2A/p16(INK4A), but no SMAD4/DPC4 mutations or microsatellite instability. Both have neuroendocrine differentiation and SSTR2 receptors, precisely the features making them suitable for the therapies we propose to assay in future studies.
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