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

Jian-Ying Li1, Jun Yu2, Xu-Sheng Du3

  • 1Institute of Cancer Research, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.

Oncology Reports
|May 14, 2016
PubMed

Insights

Safflower polysaccharide (SPS) inhibits lung cancer growth by inducing apoptosis and cell cycle arrest. SPS also enhances immune activity and blocks the PI3K/Akt pathway, offering a potential new lung cancer treatment.

Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • Lung cancer is a leading cause of cancer mortality worldwide.
  • Safflower polysaccharide (SPS) shows potential in cancer treatment and immunomodulation.
  • Limited research exists on SPS's effects on lung cancer progression.

Purpose of the Study:

  • To investigate the antitumor effects of SPS on human non-small cell lung cancer (NSCLC).
  • To elucidate the underlying mechanisms of SPS's action against lung cancer.

Main Methods:

  • NSCLC cell lines (A549, YTMLC-90) were treated with SPS (0.04–2.56 mg/ml).
  • BALB/c nude mice received intraperitoneal SPS injections (15–135 mg/kg).
  • Assessed cell proliferation, apoptosis (bax, caspase-3 mRNA), cell cycle (cdc25B, cyclin B1), PI3K/Akt pathway, and immune markers (TNF-α, IL-6).

Main Results:

  • SPS suppressed NSCLC cell proliferation and induced apoptosis.
  • SPS inhibited tumor growth in vivo and caused G2/M cell cycle arrest.
  • SPS decreased Akt, p-Akt, and PI3K expression.
  • SPS enhanced immunomodulatory activities by increasing TNF-α and IL-6 levels in mice.

Conclusions:

  • SPS exhibits significant antitumor effects against human lung cancer.
  • SPS suppresses tumor growth via apoptosis induction, cell cycle arrest, and PI3K/Akt pathway inhibition.
  • SPS enhances anti-tumor immunity, suggesting its potential as a therapeutic agent for lung cancer.

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