Tanshinone IIA can inhibit human pancreatic carcinoma BxPC3 cells through decreasing the protein expressions of IGFR, EGFR, VEGFR and blocking both...

Date 29 June 2016
Event ESMO World Congress on Gastrointestinal Cancer 2016
Session ESMO World Congress on Gastrointestinal Cancer 2016 - Abstracts book
Presenter C.C. Su
Citation Annals of Oncology (2016) 27 (2): 1-85. 10.1093/annonc/mdw199
Authors C.C. Su
  • Changua Christian Hospital, Changhua, Taiwan, /

Abstract

Tanshinone IIA (Tan-IIA; C19H18O3) is derived from the roots of Radix Salviae miltiorrhizae, with anti-inflammatory activities and antioxidant properties. Our previous studies showed that Tan-IIA can inhibit human pancreatic cancer BxPC-3 cells through decreasing protein expressions of TCTP, MCL-1 and Bcl-xL but increasing Bax expression to induce apoptosis, Tan-IIA also can induce apoptosis to inhibit BxPC-3 cells through increase inducing ER stress in vitro. It was well documented that the transmembrane tyrosine kinase has been strongly implicated in the survival, growth and metastasis of many human cancers. Both RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways represent important signal transduction mechanisms and are the most frequently dysregulated kinase cascades that facilitate the proliferation and survival of cancers driven by growth factor receptors, such as epidermal growth factor receptor (EGFR), insulin-like growth factor 1 (IGF-1) receptor (IGFR) or vascular epidermal growth factor receptor (VEGFR). These signaling cascades either through epigenetic modification or somatic mutation contributing to resistance to anticancer therapies or tumorigenesis are frequently in cancer. The efficacy for Tan-IIA to inhibit pancreatic cancer still needs to be explored further. In the present study, we investigated the efficacy and molecular mechanisms in BxPC3 cells xenograft tumors and the protein expression levels of IGFR, EGFR, VEGFR, Ras, Raf, MEK, ERK, PI3K, AKT and mTOR in BxPC-3cells were treated with Tan-IIA both in vitro and in vivo.