ArticleBioscience reports2019
Qigesan reduces the motility of esophageal cancer cells via inhibiting Gas6/Axl and NF-κB expression.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Association of Serum AXL and Gas6 Levels with Clinical Outcomes in Non-Hodgkin Lymphoma Patients with Post-Chemotherapy Infection.Infection and drug resistance · 2026Article
- Knockdown of Gas6 Exerts Anti-Esophageal Cancer Effects by Inhibiting the PI3K/AKT Pathway.Current issues in molecular biology · 2024Article
- Association of lung-intestinal microecology and lung cancer therapy.Chinese medicine · 2023Review
- Gas6/AXL pathway: immunological landscape and therapeutic potential.Frontiers in oncology · 2023Review
- Natural Products for Esophageal Cancer Therapy: From Traditional Medicine to Modern Drug Discovery.International journal of molecular sciences · 2022Review
- AXL Inhibits Proinflammatory Factors to Relieve Rheumatoid Arthritis Pain by Regulating the TLR4/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Chinese Medicine Formula Siwu-Yin Inhibits Esophageal Precancerous Lesions by Improving Intestinal Flora and Macrophage Polarization.Frontiers in pharmacology · 2022Article
- Article
- Traditional Chinese Medicine Therapy for Esophageal Cancer: A Literature Review.Integrative cancer therapiesReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study is mainly to explore the mechanism that how Qigesan (QGS) affects the movement capacity of esophageal cancer (EC) cell. QGS incubates ECA109 and TE1 cell lines and detecting the motility of tumor cells by different experiments. Growth arrest-specific 6 (Gas6) and Anexelekto (Axl) were co-localized, and then detecting Gas6, Axl signaling pathway, and protein expression after QGS intervention. Similarly, Observing the signal localization and protein expression of P-phosphoinositide3-kinases (PI3K), P-AKT protein kinase B (AKT), P-nuclear factor-kappa B (NF-κB), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9). The results showed that the concentration of QGS was less than 200 ug/ml, and the cultured cells did not exceed 24 h, that no obvious cytotoxicity was observed. QGS significantly inhibited the mobility of ECA109 and TE1 cell lines in the concentration-dependent manner. In addition, QGS can regulate the Gas6/Axl pathway, inhibit the formation and localization of the Gas6/Axl complex, and reduce the protein activation of PI3K/AKT, NF-κB, MMP2, and MMP9. Experimental innovation shows that QGS can significantly slow down the mobility of EC cells by regulating the Gas6/Axl complex and downstream signaling pathways, and provides a theoretical basis for the pharmacological effects of QGS in the therapy of EC.
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