Safflower polysaccharide induces NSCLC cell apoptosis by inhibition of the Akt pathway

Oncol Rep. 2016 Jul;36(1):147-54. doi: 10.3892/or.2016.4784. Epub 2016 May 4.


Lung cancer is the leading cause of cancer death in the world. Safflower polysaccharide (SPS) has been used for the improvement of immunomodulatory activities and treatment of cancers. However, studies on the effect of SPS on the progression of lung cancer have rarely been reported. To study the antitumor effect of SPS on human lung cancer and its potential mechanism, non-small cell lung cancer cell lines (NSCLC), A549 and YTMLC-90 were treated with SPS at various concentrations ranging from 0.04 to 2.56 mg/ml and BALB/c nude tumor-bearing mice were injected intraperitoneally with SPS at concentrations ranging from 15 to 135 mg/kg. Results showed that SPS suppressed the proliferation of A549 and YTMLC-90 cells and induced apoptosis by increasing mRNA levels of bax and caspase-3, and inhibited tumor growth in vivo. SPS induced cell cycle arrest in the G2/M phase by decreasing the expression of cdc25B and cyclin B1. Moreover, SPS decreased the expression of Akt, p-Akt and PI3K. In mice, SPS injection enhanced immunomodulatory activities by increasing levels of TNF-α and IL-6 in tumor-bearing mice. Our findings suggest that SPS suppresses tumor growth by enhancing immunomodulatory activities and blocking the PI3K/Akt pathway. This study provides new insight into the anticancer mechanism of SPS.

MeSH terms

  • A549 Cells
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Carthamus tinctorius / metabolism*
  • Caspase 3 / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclin B1 / metabolism
  • G2 Phase Cell Cycle Checkpoints / drug effects
  • Humans
  • Interleukin-6 / metabolism
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / pathology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Phosphatidylinositol 3-Kinases / metabolism
  • Plant Preparations / pharmacology*
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-akt / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Xenograft Model Antitumor Assays
  • bcl-2-Associated X Protein / metabolism
  • cdc25 Phosphatases / metabolism


  • Antineoplastic Agents
  • CCNB1 protein, human
  • Cyclin B1
  • Interleukin-6
  • Plant Preparations
  • Tumor Necrosis Factor-alpha
  • bcl-2-Associated X Protein
  • interleukin-6, mouse
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • CDC25B protein, human
  • cdc25 Phosphatases
  • Caspase 3