Your browser doesn't support javascript.
loading
Ginsenoside Rh1 regulates gastric cancer cell biological behaviours and transplanted tumour growth in nude mice via the TGF-ß/Smad pathway.
Yang, Zhiwen; Wu, Xinlin; Shen, Junjie; Gudamu, A; Ma, Yongxiang; Zhang, Zishu; Hou, Mingxing.
Afiliación
  • Yang Z; Nanjing University of Chinese Medicine, Nanjing, China.
  • Wu X; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
  • Shen J; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
  • Gudamu A; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
  • Ma Y; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
  • Zhang Z; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
  • Hou M; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Clin Exp Pharmacol Physiol ; 49(12): 1270-1280, 2022 12.
Article en En | MEDLINE | ID: mdl-36054718
Gastric cancer (GC) is one of the most prevalent malignancies of the digestive tract. Ginsenoside Rh1 was reported to exert effects on GC. The current study set out to explore the mechanism underlying Ginsenoside Rh1 effects on GC. With oxaliplatin (OXA) serving as the positive control, human GC cells AGS were treated with 0, 10, 25, 50, 74, or 100 µM of ginsenoside Rh1 for 48 h. Proliferation, migration, invasion, and apoptosis were subsequently assessed by means of MTT, scratch test, Transwell, and TUNEL, respectively. AGS cells were further jointly treated with Rh1 and the TGF-ß/Smad pathway activator Kartogenin, followed by detection of TGF-ß/Smad pathway effects on AGS biological behaviours. Moreover, TGF-ß/Smad pathway activation was detected with a Western blot assay. Furthermore, xenograft tumour models were established and tumour growth was recorded. Ki-67 expression patterns and apoptosis were detected with immunohistochemistry and TUNEL, respectively. In vitro, Ginsenoside Rh1 repressed AGS cell proliferation, migration, and invasion, and further promoted apoptosis, with a concentration of 50 µM Rh1 exerting the equivalent effects as OXA. In vivo, Ginsenoside Rh1 inhibited GC proliferation and induced tumour cell apoptosis. Mechanistically, Ginsenoside Rh1 reduced TGF-ß1 and TGF-ß2 levels and Smad2 and Smad3 phosphorylation levels. Collectively, our findings highlighted that ginsenoside Rh1 inhibited GC cell growth and tumour growth in xenograft tumour models via inhibition of the TGF-ß/Smad pathway.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Gástricas / Ginsenósidos Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Clin Exp Pharmacol Physiol Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Gástricas / Ginsenósidos Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Clin Exp Pharmacol Physiol Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia