Home Neoplasma Ahead of print Neoplasma Vol.69, No.5, p.1101–1107, 2022

Journal info


6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.69, No.5, p.1101–1107, 2022

Title: SPARC induces M2 polarization of macrophages to promote proliferation, migration, and angiogenesis of cholangiocarcinoma cells
Author: Shi-Kang Deng, Yun Jin, Yan Jin, Jun-Feng Wang

Abstract: Cholangiocarcinoma (CCA) is a disease that includes a variety of epithelial neoplasms characterized by the differentiation of cholangiocytes. M2 polarization is imperative to the development of CCA cells. In this study, we investigated the influence of secreted protein acidic and rich in cysteine (SPARC) on M2 polarization and CCA cell growth. We found that the SPARC level was amplified in M2-polarized macrophages and TAMs. In addition, the downregulation of SPARC prevented the M2 polarization of macrophages. Silencing SPARC inhibited the M2 macrophage-mediated effects on the proliferation, migration, and angiogenesis of CCA cells. Additionally, SPARC knockdown blocked the M2 polarization of macrophages by inhibiting the PI3K/AKT signaling. Moreover, an activator of PI3K signaling repressed the effect of SPARC knockdown on the M2 macrophage-induced elevation of proliferation, migration, and angiogenesis in CCA cells. In conclusion, SPARC contributes to the M2 polarization of macrophages to promote proliferation, migration, and angiogenesis of CCA cells, which provides new insight into the treatment of CCA.

Keywords: cholangiocarcinoma; SPARC; M2 polarization; PI3K/AKT signaling
Published online: 11-Aug-2022
Year: 2022, Volume: 69, Issue: 5 Page From: 1101, Page To: 1107
doi:10.4149/neo_2022_220324N333


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.