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Differential anti-tumor activities of curcumin against Ras- and Src-activated human adenocarcinoma cells

Misaki Ono1, Takako Higuchi, Mikako Takeshima

  • 1Graduate School of Health and Nutritional Sciences, Nakamura Gakuen University, 5-7-1 Befu, Johnan-ku, Fukuoka, Fukuoka 814-0198, Japan.

Biochemical and Biophysical Research Communications
|June 4, 2013
PubMed

Insights

Curcumin

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Curcumin is a potential anticancer agent targeting multiple signaling pathways.
  • The influence of oncogenic Src and Ras on curcumin sensitivity is not well understood.

Purpose of the Study:

  • To investigate the role of activated Src and Ras oncogenes in modulating curcumin sensitivity in human adenocarcinoma cells.
  • To elucidate the specific molecular mechanisms underlying curcumin's effects in the presence of these oncogenes.

Main Methods:

  • HAG-1 human adenocarcinoma cells were transfected with activated Src or Ras.
  • Cellular responses to curcumin, including cell cycle progression, apoptosis, and key signaling pathway modulation (Erk1/2, Akt, mTOR, S6K1, PARP, Bcl-xL, Bax), were analyzed.

Main Results:

  • Activation of Src or Ras did not confer curcumin resistance.
  • Curcumin inhibited Akt signaling universally but enhanced Erk1/2 primarily in Ras-activated cells.
  • Apoptosis induction (PARP cleavage) was most pronounced in Src-activated cells, with altered Bcl-xL and Bax expression.
  • G2/M cell cycle arrest was significantly increased in Ras-activated cells, linked to Erk1/2 activation.

Conclusions:

  • Curcumin's anticancer effects are mechanistically distinct in Src-driven versus Ras-driven cancers.
  • Growth inhibition in Ras-driven cancers is mainly via G2/M arrest, while Src-driven cancers undergo apoptosis.
  • These findings provide a rationale for using curcumin in specific human cancer contexts based on oncogene activation.

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