AQP1 knockdown inhibits hepatocellular carcinoma growth and invasion and weakens the oncogenic activity of exosomal GPC1 in a mouse model
- 1Department of Interventional Radiology, The First Affiliated Hospital of Bengbu Medical University
- 2Department of General Practice, The First Affiliated Hospital of Bengbu Medical University
Abstract
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.
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BibTeX
@article{qian2026aqp1,
title = {{AQP1 knockdown inhibits hepatocellular carcinoma growth and invasion and weakens the oncogenic activity of exosomal GPC1 in a mouse model}},
author = {Jingyu Qian and Xiaoyun Tang and Longji Ye and Panpan Jin and Zhongqiang Qin and Rongxin Wang and Hongyan Guo and Miao Li},
journal = {Scientific Reports},
year = {2026},
month = jul,
doi = {10.1038/s41598-026-59201-7},
url = {https://doi.org/10.1038/s41598-026-59201-7},
note = {CC BY},
}
RIS
TY - JOUR
TI - AQP1 knockdown inhibits hepatocellular carcinoma growth and invasion and weakens the oncogenic activity of exosomal GPC1 in a mouse model
AU - Jingyu Qian
AU - Xiaoyun Tang
AU - Longji Ye
AU - Panpan Jin
AU - Zhongqiang Qin
AU - Rongxin Wang
AU - Hongyan Guo
AU - Miao Li
PY - 2026
DA - 2026/07/01
JO - Scientific Reports
DO - 10.1038/s41598-026-59201-7
UR - https://doi.org/10.1038/s41598-026-59201-7
AB - 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.
SN - 2045-2322
ER -