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Phellinus linteus sensitises apoptosis induced by doxorubicin in prostate cancer

L Collins1, T Zhu, J Guo

  • 1Department of Pathology, K522, Boston University School of Medicine, 80 East Concord Street, Boston, MA 02118, USA.

British Journal of Cancer
|July 27, 2006
PubMed

Insights

Phellinus linteus (PL) mushroom extract synergizes with doxorubicin to induce apoptosis in prostate cancer cells by activating caspases and JNK. This combination therapy shows potential for enhancing anticancer drug efficacy.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Phellinus linteus (PL) mushroom exhibits antitumour properties, primarily due to its polysaccharide content.
  • The precise mechanisms underlying PL's anticancer effects are not fully understood.
  • Doxorubicin (Dox), an anticancer drug, induces apoptosis through caspase cascade activation.

Purpose of the Study:

  • To investigate the effect of Phellinus linteus on doxorubicin-induced apoptosis in LNCaP prostate cancer cells.
  • To elucidate the molecular mechanisms involved in the combined treatment's apoptotic effects.
  • To assess the therapeutic potential of PL in combination with conventional anticancer agents.

Main Methods:

  • Prostate cancer LNCaP cells were treated with Phellinus linteus (PL) and/or doxorubicin (Dox) at low doses.
  • Apoptosis induction was assessed, along with caspase cleavage (caspases 8, 3, BID) and JNK activation.
  • The role of JNK and caspase pathways was evaluated using a caspase inhibitor (z-VADfmk) and JNK suppression.

Main Results:

  • Low doses of PL or Dox alone did not induce significant apoptosis.
  • Combination treatment with low-dose PL and Dox demonstrated a synergistic induction of apoptosis.
  • The synergistic apoptosis involved the cleavage of caspases 8, 3, and BID, and was blocked by z-VADfmk.
  • JNK activation was observed with PL or combination treatment, and its partial suppression reduced apoptosis.

Conclusions:

  • Phellinus linteus synergizes with doxorubicin to enhance apoptosis in prostate cancer cells.
  • The combination treatment activates caspase-dependent pathways and involves JNK signaling.
  • PL holds therapeutic potential for augmenting the efficacy of prostate cancer drugs.

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