Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells

BMC Complement Altern Med. 2019 Aug 7;19(1):204. doi: 10.1186/s12906-019-2601-x.

Abstract

Background: Metastasis is the main cause of lung cancer death. As a seed of metastasis, circulating tumor cells are an important target for metastasis intervention. The traditional Chinese medicine, Jinfukang, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). In this study, we investigated the action and underlying mechanisms of Jinfukang against circulating lung tumor cells.

Methods: The cell counting kit-8 (CCK-8), colony formation and cell cycle assays were used to study the cell proliferation ability. Flow cytometry was used to detect the apoptosis and the expression level of ROS and Caspase-3. Comet and TUNEL assays were used to detect DNA damage. DNA damage related pathway protein was detected by western blot.

Results: Jinfukang significantly inhibits the proliferation of CTC-TJH-01 cells by inducing G1 phase arrest and inhibits their colony formation in a dose-dependent manner. Moreover, Jinfukang induces apoptosis in CTC-TJH-01 cells through the ROS-mediated ATM/ATR-p53 pathway and DNA damage.

Conclusions: Our findings suggest that Jinfukang may be a potential drug for lung cancer metastasis.

Keywords: Apoptosis; Circulating tumor cell; Jinfukang; Non-small cell lung cancer; Oxidative stress.

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects
  • Ataxia Telangiectasia Mutated Proteins / genetics
  • Ataxia Telangiectasia Mutated Proteins / metabolism
  • Carcinoma, Non-Small-Cell Lung / drug therapy
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / physiopathology
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • DNA Damage / drug effects*
  • Drugs, Chinese Herbal / pharmacology*
  • Humans
  • Neoplastic Cells, Circulating / drug effects*
  • Neoplastic Cells, Circulating / metabolism
  • Oxidative Stress / drug effects*
  • Reactive Oxygen Species / metabolism
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Antineoplastic Agents, Phytogenic
  • Drugs, Chinese Herbal
  • Reactive Oxygen Species
  • Tumor Suppressor Protein p53
  • jinfukang
  • Ataxia Telangiectasia Mutated Proteins