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<p>The development of hepatocellular carcinoma may be regulated by exosome-mediated cell-cell communication. GPC1-enriched exosomes have been associated with malignant phenotypes, while AQP1 has been related to tumor development and metastasis. The functional association of AQP1 and exosomal GPC1 in vivo remains to be clarified. Co-immunoprecipitation was applied to test the interaction of AQP1 with exosomal GPC1 in HCC cells. We generated a mouse xenograft model using control cells and AQP1 knockdown cells, with or without treatment with GPC1-high exosomes. Tumor growth was monitored by longitudinal caliper measurements and endpoint tumor weight. Histology and molecular characteristics were profiled using H&amp;E staining, immunofluorescence, and immunohistochemistry. The proteins associated with ERK and MEK signaling pathways were detected through western blotting. Co-immunoprecipitation of AQP1 and GPC1 demonstrated a recovery of AQP1 and exosomal GPC1 in the same protein complex. AQP1 knockdown was accompanied by reduced xenograft tumor growth, and diminished tumor-promoting effect of GPC1-high exosomes. Tissue examinations revealed coordinated alterations in marker expression and proliferative state in all treatment groups. Total ERK and total MEK were largely similar across groups; phospho-ERK and phospho-MEK display condition-specific differences. Tumor AQP1 staining was markedly greater than that of peritumoral tissue. These data suggest that the AQP1 status may influence tumor sensitivity to GPC1 enriched exosomal stimulation in vivo, and suggest that further analysis of AQP1 as an effector in exosome related oncogenic activity in HCC is warranted. </p>

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AQP1 knockdown inhibits hepatocellular carcinoma growth and invasion and weakens the oncogenic activity of exosomal GPC1 in a mouse model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月19日

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  • Jingyu Qian,
  • Xiaoyun Tang,
  • Longji Ye,
  • Panpan Jin,
  • Zhongqiang Qin,
  • Rongxin Wang,
  • Hongyan Guo,
  • Miao Li

摘要

The development of hepatocellular carcinoma may be regulated by exosome-mediated cell-cell communication. GPC1-enriched exosomes have been associated with malignant phenotypes, while AQP1 has been related to tumor development and metastasis. The functional association of AQP1 and exosomal GPC1 in vivo remains to be clarified. Co-immunoprecipitation was applied to test the interaction of AQP1 with exosomal GPC1 in HCC cells. We generated a mouse xenograft model using control cells and AQP1 knockdown cells, with or without treatment with GPC1-high exosomes. Tumor growth was monitored by longitudinal caliper measurements and endpoint tumor weight. Histology and molecular characteristics were profiled using H&E staining, immunofluorescence, and immunohistochemistry. The proteins associated with ERK and MEK signaling pathways were detected through western blotting. Co-immunoprecipitation of AQP1 and GPC1 demonstrated a recovery of AQP1 and exosomal GPC1 in the same protein complex. AQP1 knockdown was accompanied by reduced xenograft tumor growth, and diminished tumor-promoting effect of GPC1-high exosomes. Tissue examinations revealed coordinated alterations in marker expression and proliferative state in all treatment groups. Total ERK and total MEK were largely similar across groups; phospho-ERK and phospho-MEK display condition-specific differences. Tumor AQP1 staining was markedly greater than that of peritumoral tissue. These data suggest that the AQP1 status may influence tumor sensitivity to GPC1 enriched exosomal stimulation in vivo, and suggest that further analysis of AQP1 as an effector in exosome related oncogenic activity in HCC is warranted.