As one of the most lethal and untreatable types of cancer so far, pancreatic cancer is not benefitting from advancements in research. Despite all the efforts, this malignancy is still very difficult to diagnose in time, resistant to treatments, and prone to relapses. The appearance of metastasis-notoriously difficult to fight and a signal of unfortunate prognosis-is the event most dreaded by every cancer patient, especially by those with pancreatic cancer. Strategies for early detection and treatment of metastases are limited, and new action plans are desperately awaited. Recently, the importance of cell-secreted vesicles, or exosomes, in cell-cell communication and, particularly, their key role in promoting pathological conditions, such as infectious diseases and cancer, have attracted the attention of the scientific community. The discovery of some exosome membrane components, such as adhesion receptors and integrins, and their ability to influence cancer cell functions and metastasis progression, has added some important understanding of the metastatic process and will hopefully open the door to the development of new tools for identifying and targeting metastases. The aim of this review is to discuss the role played by integrins in exosomal-mediated pancreatic cancer progression and metastasis.
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http://dx.doi.org/10.1016/j.canlet.2021.03.010 | DOI Listing |
J Clin Invest
January 2025
Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Metabolic reprogramming shapes tumor microenvironment (TME) and may lead to immunotherapy resistance in pancreatic ductal adenocarcinoma (PDAC). Elucidating the impact of pancreatic cancer cell metabolism in the TME is essential to therapeutic interventions. "Immune cold" PDAC is characterized by elevated lactate levels resulting from tumor cell metabolism, abundance of pro-tumor macrophages, and reduced cytotoxic T cell in the TME.
View Article and Find Full Text PDFFront Oncol
January 2025
Angiogenesis Group, Center for Biomedical Research of La Rioja (CIBIR), Logroño, Spain.
[This corrects the article DOI: 10.3389/fonc.2024.
View Article and Find Full Text PDFOnco Targets Ther
January 2025
Department of Pharmacology, adMare BioInnovations, Montréal, Quebec, H4S 1Z9, Canada.
The gene is nearly ubiquitously subjected to activating mutation in pancreatic adenocarcinomas (PDAC), occurring at a frequency of over 90% in tumors. Mutant KRAS drives sustained signaling through the MAPK pathway to affect frequently disrupted cancer phenotypes including transcription, proliferation and cell survival. Recent research has shown that PDAC tumor growth and survival required a guanine nucleotide exchange factor for RAS homolog family member A (RhoA) called GEF-H1.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Surgery, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Pancreatic cancer (PC) remains one of the most lethal malignancies, primarily due to its intrinsic resistance to conventional therapies. MicroRNAs (miRNAs), key regulators of gene expression, have been identified as crucial modulators of drug resistance mechanisms in this cancer type. This review synthesizes recent advancements in our understanding of how miRNAs influence treatment efficacy in PC.
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