Radiation-triggerable bioreactors enable bioenergetic reprograming of cancer stem cell plasticity via targeted arginine metabolism disruption for augmented radio-immunotherapy

Biomaterials. 2025 Nov:322:123391. doi: 10.1016/j.biomaterials.2025.123391. Epub 2025 May 5.

Abstract

Cancer stem cells (CSCs) are a major cause for the insufficient tumor eradication in the clinic, which universally present enhanced mitochondrial oxidative phosphorylation (OXPHOS) to facilitate stemness maintenance and drive treatment resistance. Herein, we report a nanointegrative radiation-triggerable bioreactor (RTB) that selectively remodels CSC-intrinsic arginine metabolism to bioenergetically reprogram CSCs towards a therapeutically-vulnerable differentiated state, leading to durable radio-immunotherapeutic responses in vivo. The RTB nanosystem was developed through the supramolecular integration of radioresponsive iNOS-expressing genetic circuits (pDNAiNOS) and β-lapachone (LAP) into CSC-targeting cationic liposomes. Low-dose radiotherapy (LDR)-induced Nrf2 upregulation readily activates pDNAiNOS to express excessive iNOS, which then depletes CSC-intrinsic arginine while generating abundant nitric oxide (NO) for in-situ amplification of LDR-mediated cytotoxicity. Meanwhile, LDR also upregulates NQO1 expression to promote LAP-mediated ROS generation. These effects could act in a cooperative manner to potently damage CSC mitochondria, which not only blocks OXPHOS activity to drive the differentiation of CSCs for abolishing their self-renewal and resistance capability, but also enhances their propensity towards immunogenic necroptosis to elicit adaptive antitumor immunity, showing significant potential for treating therapy-persistent tumors.

Keywords: Arginine metabolism disruption; Cancer stem cell therapy; Mitochondrial bioenergetic reprogramming; Necroptosis; Radio-immunotherapy.

MeSH terms

  • Animals
  • Arginine* / metabolism
  • Bioreactors*
  • Cell Line, Tumor
  • Energy Metabolism / radiation effects
  • Humans
  • Immunotherapy* / methods
  • Mice
  • Mitochondria / metabolism
  • Neoplastic Stem Cells* / metabolism
  • Neoplastic Stem Cells* / pathology
  • Neoplastic Stem Cells* / radiation effects
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Oxidative Phosphorylation
  • Reactive Oxygen Species / metabolism

Substances

  • Arginine
  • Nitric Oxide Synthase Type II
  • Nitric Oxide
  • Reactive Oxygen Species