Open AccessMACC1 overexpression in carcinoma‑associated fibroblasts induces the invasion of lung adenocarcinoma cells via paracrine signaling
Author(s) -
Zhuoshi Li,
Tao Guo,
Fang Lei,
Nan Li,
Xiaochao Wang,
Peng Wang,
Shilei Zhao,
Fengzhou Li,
Yanwei Cui,
Xin Shu,
Lei Zhao,
Jinxiu Li,
Zhuoshi Li
Publication year - 2019
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2019.4702
Subject(s) - paracrine signalling , adenocarcinoma , cancer research , autocrine signalling , biology , pathology , oncogene , metastasis , lung cancer , cell , cancer , cell cycle , medicine , cell culture , receptor , biochemistry , genetics
Carcinoma‑associated fibroblasts (CAFs) are essential for initiating lung cancer cell invasion and metastasis. An elevated MACC1 expression has been implicated in the progression of lung adenocarcinoma. Hitherto, the role of MACC1 in lung adenocarcinoma‑derived CAFs remains unclear. In this study, CAFs isolated from the tissues of patients with lung adenocarcinoma expressed typical CAF markers (shown by immunohistochemical and immunofluorescence analysis) and exhibited enhanced migration and invasion abilities when co‑cultured with A549 cells in a microfluidic model. MACC1‑overexpressing CAFs not only demonstrated an increased invasion, but also exerted a promoting effect on the invasion of tumor cells. The reduced expression of MACC1 impaired the invasive ability of the CAFs. Western blot analysis and RT‑qPCR analysis demonstrated that multiple paracrine pathways were activated in the MACC1‑overexpressing CAFs. Overall, this study presents a novel role of MACC1 in CAF‑induced lung adenocarcinoma cell invasion, which possibly occurs via paracrine signaling. Furthermore, MACC1 was indicated to be a potential therapeutic target for lung adenocarcinoma.