Paclitaxel-induced apoptosis in MCF-7 breast-cancer cells

Int J Cancer. 1997 Jan 17;70(2):214-20. doi: 10.1002/(sici)1097-0215(19970117)70:2<214::aid-ijc13>3.0.co;2-i.

Abstract

A study of MCF-7 human breast cancer cells was undertaken to ascertain the degree of apoptosis induction by paclitaxel and if the induction of apoptosis could be enhanced by caffeine. Paclitaxel (0-20 ng/ml) caused concentration-dependent increases in morphologically identifiable apoptotic cells (up to 43% of cell population) and cells with DNA strand breaks (up to 38%), a commonly cited marker of apoptosis. Maximal DNA strand breakage occurred after 16 hr of exposure to paclitaxel and maximal apoptotic-appearing cells occurred after 24 hr. The remaining non-apoptotic paclitaxel-exposed cells were growth arrested in G2. A 4-hr exposure to caffeine concentration-dependently (0-20 mM) increased apoptosis to 88% of the cell population. Our results show induction of apoptosis in breast cancer cells by paclitaxel, and enhancement of this process by caffeine.

MeSH terms

  • Adenocarcinoma / pathology*
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects*
  • Breast Neoplasms / pathology*
  • Caffeine / pharmacology
  • Cell Cycle
  • Cisplatin / pharmacology
  • Cytarabine / pharmacology
  • DNA Damage
  • DNA Fragmentation
  • DNA, Neoplasm / drug effects
  • Doxorubicin / pharmacology
  • Estrogens*
  • Female
  • Humans
  • Neoplasms, Hormone-Dependent / pathology*
  • Paclitaxel / pharmacology*
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • Antineoplastic Agents, Phytogenic
  • DNA, Neoplasm
  • Estrogens
  • Cytarabine
  • Caffeine
  • Doxorubicin
  • Paclitaxel
  • Cisplatin