title: Inhibitory effects of Guben Yiliu Formula II (II) and its blood activation prescriptions on the growth of MCF-7 human breast cancer xenografts in nude mice.
abstract: OBJECTIVE
  To investigate the inhibitory effects of Guben Yiliu Formula II(II, GFII) and its blood activation prescription (BAP) on the growth of MCF-7 human breast cancer xenografts in nude mice, and explore their mechanisms of action.
  
  
  METHODS
  After the establishment of the MCF-7 human breast cancer xenograft model in nude mice, the mice in the GFII and BAP groups were administered with GFII (6.56 g/mL) and BAP (1.65 g/mL) by gavage for 28 days, respectively. The tumor volume and weight were measured twice a week throughout the treatment period. Apoptotic cells were identified by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. The expression of microtubule associated protein 1 light chain 3 (LC3) was examined by immunohistochemistry, and Western blotting analysis was performed to detect the expression of anti-apoptotic protein Bcl-2 and LC3, as well as the effects on phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway.
  
  
  RESULTS
  Compared with the control group, the GFII and BAP groups could significantly inhibit the growth of MCF-7 human breast cancer xenografts in nude mice. The expression of Bcl-2 protein was lower in the GFII and BAP than in the control group, whereas both the percentage of apoptotic cells and LC3-II/LC3-I ratio were higher than in the control group. In addition, significantly reduced expression of phospho-Akt, phosphor-mTOR and mTOR were observed in the blood activation group (P<0.05).
  
  
  CONCLUSIONS
  To some extent, the GFII and its BAP can exert their inhibitory effect on the growth of MCF-7 human breast cancer xenografts by inducing the cell apoptosis and autophagy. In addition to the induction of cell apoptosis, we also found that the BAP of GFII could induce cell autophagy by inhibiting of PI3K/Akt/mTOR signaling pathway, and then suppress the breast cancer cell growth.
authors.affiliation: Department of Hematology and Oncology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100070, China.
authors.forename: Cong
authors.initials: C
authors.lastname: Ma
authors.forename: Xiao-Min
authors.initials: XM
authors.lastname: Wang
authors.forename: Ming-Wei
authors.initials: MW
authors.lastname: Yu
authors.forename: Gan-Lin
authors.initials: GL
authors.lastname: Zhang
authors.forename: Nan
authors.initials: N
authors.lastname: Nan
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.forename: Ke-Xin
authors.initials: KX
authors.lastname: Cao
authors.forename: Jin-Ping
authors.initials: JP
authors.lastname: Li