Open AccessRetracted: GNA 13 promotes tumor growth and angiogenesis by upregulating CXC chemokines via the NF ‐κB signaling pathway in colorectal cancer cells
Author(s) -
Zhang Zhongqiang,
Tan Xiao,
Luo Jing,
Cui Beibei,
Lei Sanlin,
Si Zhongzhou,
Shen Liangfang,
Yao Hongliang
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1783
Subject(s) - angiogenesis , chemokine , cancer research , signal transduction , downregulation and upregulation , metastasis , cancer , nf κb , colorectal cancer , biology , epithelial–mesenchymal transition , immunology , inflammation , microbiology and biotechnology , biochemistry , gene , genetics
GNA 13 has been found overexpressed in various types of cancer, which is related to tumor metastasis and progression. However, the biological functions of GNA 13 in colorectal cancer ( CRC ) progression remain unclear. This study aimed to explore the role of GNA 13 in CRC and investigate the mechanism of how GNA 13 promotes tumor growth. Interestingly, our findings showed that GNA 13 is commonly upregulated in CRC , where these events are associated with a worse histologic grade and poor survival. Increased expression levels of GNA 13 promoted cell growth, migration, invasion, and epithelial‐mesenchymal transition, whereas GNA 13 silencing abrogated these malignant phenotypes. In addition, overexpressing GNA 13 in cancer cells increased the levels of the chemokines CXCL 1, CXCL 2, and CXCL 4, which contributed to CRC proliferation and colony formation. Moreover, our mechanistic investigations suggest that the NF ‐κB/p65 signaling pathway was activated by the increase in GNA 13 levels. Inhibiting the NF ‐κB/p65 pathway with an inhibitor decreased GNA 13‐induced migration, invasion and CXCL chemokine level increases, indicating the critical role of NF ‐κB/p65 signaling in mediating the effects of GNA 13 in CRC . Together, these results demonstrate a key role of GNA 13 overexpression in CRC that contributes to malignant behavior in cancer cells, at least in part through stimulating angiogenesis and increasing the levels of the NF ‐κB‐dependent chemokines CXCL 1, CXCL 2, and CXCL 4.