Open AccessLong non‐coding RNA FOXP 4‐ AS 1 is an unfavourable prognostic factor and regulates proliferation and apoptosis in colorectal cancer
Author(s) -
Li Juan,
Lian Yifan,
Yan Changsheng,
Cai Zeling,
Ding Jie,
Ma Zhonghua,
Peng Peng,
Wang Keming
Publication year - 2017
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12312
Subject(s) - gene knockdown , flow cytometry , biology , cell growth , apoptosis , cancer research , oncogene , colorectal cancer , long non coding rna , cell culture , in vivo , cell cycle , cancer , downregulation and upregulation , microbiology and biotechnology , gene , genetics
Objectives Despite improvements in diagnosis and treatment, colorectal cancer ( CRC ) remains the third most common malignancy, and fourth‐leading cause of cancer‐related death worldwide, and has a particularly high incidence in Western countries. Recent studies have suggested that long non‐coding RNA s (lnc RNA s) compose a novel class of regulators of cancer biological processes, such as proliferation, apoptosis and metastasis. Here, we report that lnc RNA FOXP 4‐ AS 1 acts as a functional oncogene in CRC pathogenesis. Moreover, we have attempted to investigate the effects of FOXP 4‐ AS 1 on tumour progression, both in vitro and in vivo . Materials and methods In this study, bioinformatic analyses and qPCR were performed to investigate FOXP 4‐ AS 1 expression in CRC tissue samples and CRC cell lines. We inhibited FOXP 4‐ AS 1 expression via FOXP 4‐ AS 1‐specific si RNA transfection. Cell proliferation was assessed using cell viability and colony formation assays, as well as by flow cytometry and ethynyl deoxyuridine (Edu) analyses. Apoptosis was assessed using flow cytometry. Animal tumour xenografts were generated, and immunohistochemistry ( IHC ) was performed to evaluate effects of FOXP 4‐ AS 1 on CRC tumour growth in vivo . Results We found that FOXP 4‐ AS 1 was up‐regulated in CRC tissues and cell lines and that its overexpression positively correlated with advanced pathological stages and larger tumour size. Additionally, we found that FOXP 4‐ AS 1 knockdown inhibited cell proliferation and induced apoptosis. Furthermore, FOXP 4‐ AS 1 knockdown induced marked increase in number of cells in G0/G1 phase and reduction in number of cells in S phase, in DLD ‐1, HT ‐29 and HCT 116 cell lines. Consistent with these findings, FOXP 4‐ AS 1 silencing inhibited tumour growth in vivo . Conclusion These findings suggest that FOXP 4‐ AS 1 plays a crucial role in CRC progression and may be a new biomarker in patients with CRC .