Biomedicine & Pharmacotherapy (Oct 2022)

Polyester nanomedicines targeting inflammatory signaling pathways for cancer therapy

  • Sabya Sachi Das,
  • Sandeep Kumar Singh,
  • P.R.P. Verma,
  • Rekha Gahtori,
  • Belay Zeleke Sibuh,
  • Kavindra Kumar Kesari,
  • Niraj Kumar Jha,
  • Sugapriya Dhanasekaran,
  • Vijay Kumar Thakur,
  • Ling Shing Wong,
  • Sinouvassane Djearamane,
  • Piyush Kumar Gupta

Journal volume & issue
Vol. 154
p. 113654

Abstract

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The growth of cancerous cells and their responses towards substantial therapeutics are primarily controlled by inflammations (acute and chronic) and inflammation-associated products, which either endorse or repress tumor progression. Additionally, major signaling pathways, including NF-κB, STAT3, inflammation-causing factors (cytokines, TNF-α, chemokines), and growth-regulating factors (VEGF, TGF-β), are vital regulators responsible for the instigation and resolution of inflammations. Moreover, the conventional chemotherapeutics have exhibited diverse limitations, including poor pharmacokinetics, unfavorable chemical properties, poor targetability to the disease-specific disease leading to toxicity; thus, their applications are restricted in inflammation-mediated cancer therapy. Furthermore, nanotechnology has demonstrated potential benefits over conventional chemotherapeutics, such as it protected the incorporated drug/bioactive moiety from enzymatic degradation within the systemic circulation, improving the physicochemical properties of poorly aqueous soluble chemotherapeutic agents, and enhancing their targetability in specified carcinogenic cells rather than accumulating in the healthy cells, leading reduced cytotoxicity. Among diverse nanomaterials, polyester-based nanoparticulate delivery systems have been extensively used to target various inflammation-mediated cancers. This review summarizes the therapeutic potentials of various polyester nanomaterials (PLGA, PCL, PLA, PHA, and others)-based delivery systems targeting multiple signaling pathways related to inflammation-mediated cancer.

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