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<p>Drug-eluting microspheres (DEMs) are key for transcatheter arterial chemoembolization (TACE) in advanced hepatocellular carcinoma (HCC), but face challenges like tumor multidrug resistance (MDR) and poor post-TACE outcomes. Here we show a dual-effect microsphere (PTIMS) co-encapsulating idarubicin (IDA) and tariquidar (TQR) for simultaneous chemotherapy and MDR reversal, plus minimally invasive photothermal therapy (PTT) to boost antitumor efficacy. Physicochemical tests confirm IDA/TQR loading in PTIMS, with PTT accelerating drug release. In vitro, PTIMS-PTT strongly inhibits H22 cell proliferation, migration and invasion by downregulating membrane P-glycoprotein (P-gp), promoting apoptosis and reducing IDA efflux. In vivo, it suppresses tumor growth in murine H22 models (upregulating TNF-α, downregulating Ki67/P-gp) and inhibits progression in rabbit VX2 liver tumors via robust embolization. PTIMS offers a promising strategy to enhance TACE efficacy, with high clinical translation potential.</p>

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Overcoming drug resistance microspheres combined with photothermal ablation reinforce transcatheter arterial chemoembolization of hepatocellular carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月25日

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  • Jiheng Shan,
  • Chengzhi Zhang,
  • Yiming Liu,
  • Bingtong Yue,
  • Bin Han,
  • Jing Li,
  • Guodun Zheng,
  • Kunpeng Wu,
  • Huijuan Wu,
  • Yiran Wang,
  • Qingqing He,
  • Xiaonan Shan,
  • Zongming Li,
  • Ping Wu,
  • Kewei Ren,
  • Zhen Li,
  • Jianzhuang Ren,
  • Linyong Du,
  • Yanan Zhao,
  • Xinwei Han

摘要

Drug-eluting microspheres (DEMs) are key for transcatheter arterial chemoembolization (TACE) in advanced hepatocellular carcinoma (HCC), but face challenges like tumor multidrug resistance (MDR) and poor post-TACE outcomes. Here we show a dual-effect microsphere (PTIMS) co-encapsulating idarubicin (IDA) and tariquidar (TQR) for simultaneous chemotherapy and MDR reversal, plus minimally invasive photothermal therapy (PTT) to boost antitumor efficacy. Physicochemical tests confirm IDA/TQR loading in PTIMS, with PTT accelerating drug release. In vitro, PTIMS-PTT strongly inhibits H22 cell proliferation, migration and invasion by downregulating membrane P-glycoprotein (P-gp), promoting apoptosis and reducing IDA efflux. In vivo, it suppresses tumor growth in murine H22 models (upregulating TNF-α, downregulating Ki67/P-gp) and inhibits progression in rabbit VX2 liver tumors via robust embolization. PTIMS offers a promising strategy to enhance TACE efficacy, with high clinical translation potential.