(-)‑Oleocanthal inhibits proliferation and migration by modulating Ca2+ entry through TRPC6 in breast cancer cells

R Diez-Bello1, I Jardin1, J J Lopez1

  • 1Department of Physiology (Cellular Physiology Research Group), Institute of Molecular Pathology Biomarkers, University of Extremadura, 10003 Caceres, Spain.

Insights

(-)‑oleocanthal (OLCT), derived from olive oil, selectively targets triple-negative breast cancer cells, inhibiting proliferation and migration. This natural compound shows promise as a targeted therapy with minimal impact on healthy cells.

Area of Science:

  • * Molecular Biology
  • * Oncology
  • * Pharmacology

Background:

  • * Triple-negative breast cancer (TNBC) is aggressive and lacks targeted therapies, necessitating novel treatments.
  • * Current therapies often cause severe side effects due to their impact on normal cells.
  • * There is a critical need for anti-cancer compounds with selective toxicity towards tumor cells.

Purpose of the Study:

  • * To investigate the selective anti-cancer effects of (-)‑oleocanthal (OLCT) on breast cancer cells.
  • * To determine the mechanism of OLCT's action, focusing on TRPC6 channels and calcium signaling.
  • * To evaluate OLCT's impact on both cancerous and non-tumoral breast cell lines.

Main Methods:

  • * Cell proliferation, viability, and migration assays were performed on MDA-MB-231 (TNBC), MCF7 (ER+ breast cancer), and MCF10A (non-tumoral) cell lines.
  • * Calcium (Ca2+) mobilization and TRPC6 channel expression were analyzed.
  • * TRPC6 expression silencing was used to investigate its role in OLCT's mechanism.

Main Results:

  • * OLCT selectively reduced proliferation and viability in MDA-MB-231 and MCF7 cells, sparing MCF10A cells.
  • * OLCT inhibited MDA-MB-231 cell migration without affecting MCF10A cells.
  • * OLCT induced Ca2+ entry in cancer cells via TRPC6 channels, and downregulated TRPC6 expression in MDA-MB-231 cells.

Conclusions:

  • * (-)‑oleocanthal (OLCT) demonstrates selective anti-cancer properties against triple-negative and other breast cancer cells.
  • * OLCT's mechanism involves the downregulation of TRPC6 channel expression, impacting cancer cell proliferation and migration.
  • * OLCT represents a potential therapeutic agent for breast cancer with a favorable safety profile for non-tumoral cells.

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