In:
Evidence-Based Complementary and Alternative Medicine, Wiley, Vol. 2016, No. 1 ( 2016-01)
Abstract:
Ginsenoside F 2 (F 2 ), a protopanaxdiol type of saponin, was reported to inhibit human gastric cancer cells SGC7901. To better understand the molecular mechanisms of F 2 , an iTRAQ‐based proteomics approach was applied to define protein expression profiles in SGC7901 cells in response to lower dose (20 μ M) and shorter duration (12 hour) of F 2 treatment, compared with previous study. 205 proteins were screened in terms of the change in their expression level which met our predefined criteria. Further bioinformatics and experiments demonstrated that F 2 treatment downregulated PRR5 and RPS15 and upregulated RPL26, which are implicated in ribosomal protein‐p53 signaling pathway. F 2 also inhibited CISD2, Bcl‐xl, and NLRX1, which are associated with autophagic pathway. Furthermore, it was demonstrated that F 2 treatment increased Atg5, Atg7, Atg10, and PUMA, the critical downstream effectors of ribosomal protein‐p53 signaling pathway, and Beclin‐1, UVRAG, and AMBRA‐1, the important molecules in Bcl‐xl/Beclin‐1 pathway. The 6 differentially abundant proteins, PRR5, CISD2, Bcl‐xl, NLRX1, RPS15, and RPL26, were confirmed by western blot. Taken together, ribosomal protein‐p53 signaling pathway and Bcl‐xl/Beclin‐1 pathway might be the most significantly regulated biological process by F 2 treatment in SGC7901 cells, which provided valuable insights into the deep understanding of the molecular mechanisms of F 2 for gastric cancer treatment.
Type of Medium:
Online Resource
ISSN:
1741-427X
,
1741-4288
DOI:
10.1155/ecam.v2016.1
DOI:
10.1155/2016/2635483
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2171158-6
detail.hit.zdb_id:
2148302-4
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