Research progress of plant-derived chemical compounds for overcoming pancreatic cancer drug resistance

Figure 1 Flowchart of drug resistance mechanisms in pancreatic cancer. This figure summarizes the primary mechanisms of drug resistance in pancreatic cancer. Resistance arises from extracellular matrix remodeling, overexpression of ATP-binding cassette transporters at the tumor cell membrane, intracellular defects in metabolism and DNA repair, nuclear epigenetic and gene regulatory changes, and activation of abnormal signaling pathways. These interconnected processes collectively reduce drug efficacy and facilitate tumor survival. HIF-1α: Hypoxia-inducible factor-1α; TAMs: Tumor-associated macrophages; IL: Interleukin; TGF: Transforming growth factor; MDSCs: Myeloid-derived suppressor cells; Arg1: Arginase 1; iNOS: Inducible nitric oxide synthase; ABC: ATP-binding cassette; LRP: Lung resistance-related protein; P-gp: P-glycoprotein; MRP1: Multidrug resistance-associated protein 1; hENT1: Human equilibrative nucleoside transporter 1; dCK: Deoxycytidine kinase; RRM1: Ribonucleotide reductase subunit 1; PARP: Polyadenosine-diphosphate-ribose polymerase; EMT: Epithelial-mesenchymal transition; MAL2: Myelin and lymphocyte protein 2; CSCs: Cancer stem cells; ncRNA: Non-coding RNA; lncRNA: Long non-coding RNAs; PVT1: Plasmacytoma variant translocation 1; PTEN: Phosphatase and tensin homolog; AKT: Protein kinase B; SDF-1: Stromal cell-derived factor 1; CXCR4: C-X-C receptor 4; FAK: Focal adhesion kinase; ERK: Extracellular signal-regulated kinase; STAT3: Signal transducer and activator of transcription 3.