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Understanding the molecular mechanisms that regulate pancreatic cancer stem cell formation, stemness and chemoresistance: A brief overview. | LitMetric

Understanding the molecular mechanisms that regulate pancreatic cancer stem cell formation, stemness and chemoresistance: A brief overview.

Semin Cancer Biol

Department of Hematology and Oncology, Heersink School of Medicine, University of Alabama, Birmingham, AL 35201, USA. Electronic address:

Published: January 2023

AI Article Synopsis

  • - Pancreatic cancer is highly aggressive due to its resistance to standard treatments and tendency for early spread, with cancer stem cells playing a significant role in invasiveness and drug resistance.
  • - Pancreatic cancer stem cells (PaCSCs) possess unique characteristics like high plasticity and self-renewal, impacting their metabolism and signaling pathways that contribute to their resilience against therapies.
  • - The review discusses current research on PaCSCs, their interactions with the tumor microenvironment (TME), and outlines promising new therapeutic strategies targeting these cells to improve treatment outcomes.

Article Abstract

Pancreatic cancer is one of the most aggressive cancers worldwide due to the resistances to conventional therapies and early metastasis. Recent research has shown that cancer stem cell populations modulate invasiveness, recurrence, and drug resistance in various cancers, including pancreatic cancer. Pancreatic cancer stem cells (PaCSCs) are characterized by their high plasticity and self-renewal capacities that endow them with unique metabolic, metastatic, and chemoresistant properties. Understanding the exact molecular and signaling mechanisms that underlay malignant processes in PaCSCs is instrumental for developing novel therapeutic modalities that overcome the limitations of current therapeutic regimens. In this paper, we provide an updated review of the latest research in the field and summarize the current knowledge of PaCSCs characteristics, cellular metabolism, stemness, and drug resistance. We explore how the crosstalk between the TME and PaCSCs influences stemness. We also highlight some of the key signalling pathways involved in PaCSCs stemness and drug evasion. The aim of this review is to explore how PaCSCs develop, maintain their properties, and drive tumor relapse in PC. The last section explores some of the latest therapeutic strategies aimed at targeting PaCSCs.

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Source
http://dx.doi.org/10.1016/j.semcancer.2022.12.004DOI Listing

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