Shenling Qige Granules inhibit esophageal squamous cell carcinoma progression in TE-1 xenograft and cell-based models by modulating the DCN–TGF-β/Smad signaling axis
- 1Graduate School, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, P.R. China
- 2Second Department of Oncology, The First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Hebei, P.R. China
- 3Department of Pediatric Rehabilitation, The First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Hebei, P.R. China
Abstract
Shenling Qige Granules (SLQG), derived from the Qing Dynasty formula Qige San recorded in Yi Xue Xin Wu, has been used in clinical practice in China as an adjuvant traditional Chinese medicine preparation for esophageal squamous cell carcinoma (ESCC), but its molecular basis remains unclear. This study investigated the antitumor effects and mechanisms of SLQG using TE-1 xenograft mice and SLQG-containing serum-treated TE-1 cells. Transcriptome sequencing, network pharmacology, molecular docking, molecular dynamics simulation, and public-database analysis were integrated to prioritize candidate mechanisms. Histological, molecular, cellular, and siRNA-mediated decorin (DCN) knockdown assays were performed for validation. SLQG, especially at the medium dose, inhibited xenograft tumor growth and increased DCN expression. Transcriptomic analysis highlighted the transforming growth factor-β (TGF-β)/Smad pathway. In silico analyses suggested that several SLQG-derived compounds, particularly ursolic acid, may be associated with DCN-related regulation. Public-database analysis indicated lower DCN expression in esophageal carcinoma tumor samples than in normal samples and an association with pathological stage. In vivo and in vitro, SLQG increased DCN expression, reduced Smad2/3 phosphorylation, promoted pro-apoptotic signaling, and induced G0/G1 arrest; these effects were attenuated by DCN knockdown. These findings suggest that SLQG inhibited ESCC progression in TE-1 xenograft and cell-based models, potentially through modulation of the DCN-associated TGF-β/Smad signaling axis.
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BibTeX
@article{liu2026shenling,
title = {{Shenling Qige Granules inhibit esophageal squamous cell carcinoma progression in TE-1 xenograft and cell-based models by modulating the DCN–TGF-β/Smad signaling axis}},
author = {Zihui Liu and Yiting Gu and Huanfang Fan and Mao Huang and Dehui Li and Wen Guo and Yun He and Shuang Zhang and Zhihua Du},
journal = {PLOS One},
year = {2026},
month = oct,
doi = {10.1371/journal.pone.0359405},
url = {https://doi.org/10.1371/journal.pone.0359405},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Shenling Qige Granules inhibit esophageal squamous cell carcinoma progression in TE-1 xenograft and cell-based models by modulating the DCN–TGF-β/Smad signaling axis
AU - Zihui Liu
AU - Yiting Gu
AU - Huanfang Fan
AU - Mao Huang
AU - Dehui Li
AU - Wen Guo
AU - Yun He
AU - Shuang Zhang
AU - Zhihua Du
PY - 2026
DA - 2026/10/06
JO - PLOS One
DO - 10.1371/journal.pone.0359405
UR - https://doi.org/10.1371/journal.pone.0359405
AB - Shenling Qige Granules (SLQG), derived from the Qing Dynasty formula Qige San recorded in Yi Xue Xin Wu, has been used in clinical practice in China as an adjuvant traditional Chinese medicine preparation for esophageal squamous cell carcinoma (ESCC), but its molecular basis remains unclear. This study investigated the antitumor effects and mechanisms of SLQG using TE-1 xenograft mice and SLQG-containing serum-treated TE-1 cells. Transcriptome sequencing, network pharmacology, molecular docking, molecular dynamics simulation, and public-database analysis were integrated to prioritize candidate mechanisms. Histological, molecular, cellular, and siRNA-mediated decorin (DCN) knockdown assays were performed for validation. SLQG, especially at the medium dose, inhibited xenograft tumor growth and increased DCN expression. Transcriptomic analysis highlighted the transforming growth factor-β (TGF-β)/Smad pathway. In silico analyses suggested that several SLQG-derived compounds, particularly ursolic acid, may be associated with DCN-related regulation. Public-database analysis indicated lower DCN expression in esophageal carcinoma tumor samples than in normal samples and an association with pathological stage. In vivo and in vitro, SLQG increased DCN expression, reduced Smad2/3 phosphorylation, promoted pro-apoptotic signaling, and induced G0/G1 arrest; these effects were attenuated by DCN knockdown. These findings suggest that SLQG inhibited ESCC progression in TE-1 xenograft and cell-based models, potentially through modulation of the DCN-associated TGF-β/Smad signaling axis.
SN - 1932-6203
ER -