Syringin exerts anti-breast cancer effects through PI3K-AKT and EGFR-RAS-RAF pathways

Fei Wang1, Chong Yuan1, Bo Liu2,3

  • 1Faculty of Pharmacy, Hubei University of Chinese Medicine, Wuhan, 430065, China.

Abstract

Insights

Syringin, a compound from Acanthopanax senticosus, inhibits breast cancer (BC) progression by targeting key genes like PIK3CA and HRAS. This study elucidates its anti-BC mechanisms and potential as an adjuvant therapy.

Area of Science:

  • Pharmacology
  • Bioinformatics
  • Oncology

Background:

  • Breast cancer (BC) is a leading cause of cancer mortality worldwide.
  • Syringin exhibits anti-tumor properties, but its specific anti-BC effects and mechanisms require elucidation.

Purpose of the Study:

  • To investigate the anti-breast cancer efficacy of Syringin.
  • To identify the molecular targets and pathways involved in Syringin's anti-BC action.
  • To explore Syringin's potential as an adjuvant therapy for breast cancer.

Main Methods:

  • Syringin isolation from Acanthopanax senticosus (ASH) using solvent extraction and chromatography.
  • Bioinformatic analysis to identify hub targets of Syringin against BC.
  • In vitro experiments to validate Syringin's effects on BC cell proliferation, migration, and apoptosis.

Main Results:

  • Syringin was isolated and characterized using LC-MS, NMR, and HPLC.
  • Bioinformatics identified MAP2K1, PIK3CA, HRAS, EGFR, Caspase3, and PTGS2 as hub targets.
  • PIK3CA and HRAS were linked to BC patient survival; specific ceRNA pathways were identified.
  • In vitro studies confirmed Syringin's inhibition of BC cell proliferation and migration, and promotion of apoptosis.

Conclusions:

  • Syringin exerts anti-breast cancer effects through the PI3K-AKT-PTGS2 and EGFR-RAS-RAF-MEK-ERK pathways.
  • PIK3CA and HRAS are identified as crucial hub genes for Syringin's anti-BC activity and potential adjuvant treatment.

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