Back to Journals » OncoTargets and Therapy » Volume 11

Overexpression of CLEC3A promotes tumor progression and poor prognosis in breast invasive ductal cancer

Authors Ni J, Peng Y, Yang F, Xi X, Huang X, He C

Received 2 January 2018

Accepted for publication 19 March 2018

Published 5 June 2018 Volume 2018:11 Pages 3303—3312

DOI https://doi.org/10.2147/OTT.S161311

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Justinn Cochran

Peer reviewer comments 2

Editor who approved publication: Dr Samir Farghaly


Jun Ni, Yun Peng, Fu-Lan Yang, Xun Xi, Xing-Wei Huang, Chun He

Department of Breast and Thyroid Surgery, People’s Hospital of Ganzhou City, Ganzhou, Jiangxi, People’s Republic of China

Introduction: The aim of this study was to evaluate the expression of C-type lectin domain family 3 member A (CLEC3A) and its clinical significance in breast invasive ductal cancer (IDC) as well as its effect on breast cancer (BC) cell proliferation and metastasis. In this study, the level of CLEC3A expression in The Cancer Genome Atlas (TCGA) datasets was analyzed.
Materials and methods: Clinical collected samples and BC cells were measured using quantitative reverse transcription polymerase chain reaction. Its correlations with patients’ clinicopathological characteristics were analyzed by Pearson’s chi-squared test. Overall survival (OS) analysis was performed by the Kaplan–Meier method and Cox’s proportional-hazards model. BC cell proliferation, migration, and invasion by CLEC3A knockdown were assessed using Cell Counting Kit-8 and colony formation assay, wound healing model and transwell assay, respectively, in BT474 cell line. Activities of survival factors and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling were measured by testing key molecules using Western blot assay.
Results: CLEC3A expression was markedly higher in breast IDC tissues than normal breast tissues or adjacent normal tissue. Patients with high CLEC3A expression related to higher lymph node and poorer OS of breast IDC. CLEC3A knockdown by siRNA could inhibit the BC cells BT474 proliferation, migration, and invasion, together with a decrease in expression of key proteins in survival factors and PI3K/AKT signaling pathway.
Conclusion: Elevated CLEC3A expression may correlate with breast IDC metastatic potential and indicated a poor prognosis in breast IDC. CLEC3A knockdown inhibited BC cell growth and metastasis might be through suppressing PI3K/AKT signaling activity. These findings unravel that CLEC3A is a promising therapeutic target for BC in the future.

Keywords:
breast cancer, proliferation, migration, invasion, overall survival, survival factor, PI3K/AKT

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]