Overexpression of Chemokine (C-X-C) ligand 1 (CXCL1) associated with tumor progression and poor prognosis in hepatocellular carcinoma

Abstract

BackgroundMany studies support that chemokine (C-X-C motif) ligand 1 (CXCL1) regulate tumor epithelial-stromal interactions involving in tumor growth and invasion. However, limited studies have been conducted on the expression and function of the CXCL1 gene in hepatocellular carcinoma (HCC).MethodsThe mRNA and protein level expression of CXCL1 was examined in HCC tissues and cell lines. The expression of CXCL1 was correlated with clinicopathological features and follow-up data. Overexpression approaches were used to evaluate the biological functions of CXCL1 by MTT and matrigel invasion assays. Protein expression levels of CXCL1 and P65 were determined by western blot analysis.ResultsIn this study, we found that CXCL1 expression was markedly upregulated in HCC tissues. Ectopic expression of CXCL1 significantly promoted HCC cells proliferation and invasion. Furthermore, CXCL1 promote cell invasion through NF-kB-dependent pathway. CXCL1 expression in HCC associated with clinical stage (P = 0.034) and distant metastasis (P = 0.028). Moreover, Patients with high CXCL1 expression level had poorer overall survival (OS;P = 0.027) than those with low CXCL1 expression.ConclusionsThese data indicated that the CXCL1 upregulation may contribute to both the development and progression of HCC and this effect may be associated with increased proliferation and invasiveness mainly via regulating P65 expression.

Increased expression of annexin A1 predicts poor prognosis in human hepatocellular carcinoma and enhances cell malignant phenotype

“…Immunostainings were evaluated by two experienced pathologists who were blinded to the clinical data reviewed the stained tissue sections, using the semiquantitative scoring system linking the staining intensity with the percentage of positive cells, according to the previous studies [21,22]. The intensity was classified as follows: 0, negative staining; 1, weak staining; 2, moderate staining; and 3, strong staining.…”

Diosmetin triggers cell apoptosis by activation of the p53/Bcl-2 pathway and inactivation of the Notch3/NF-κB pathway in HepG2 cells

“…Subsequently, it affects the NF-κB downstream molecules via a decrease in anti-apoptotic B-cell lymphoma (Bcl)-2 and an increase in pro-apoptotic Bcl-2-like protein 4 (Bax) and Bcl-2 homologous antagonist/killer (20). Chemokine (C-X-C motif) ligand 1 upregulation may contribute to both the development and progression of HCC, and this effect may be associated with increased proliferation and invasiveness mainly via regulating NF-κB expression (21). The mechanism of HCC metastasis may mediate through cross-talk between the NF-κB and estrogen receptor (ER) signaling pathways (22).…”

Phosphorylation of serine/arginine‐rich splicing factor 1 at tyrosine 19 promotes cell proliferation in pediatric acute lymphoblastic leukemia

“…In addition, a large number of genes are increased by the Try‐19 phosphorylation of SRSF1 (): chemokine (C‐X‐C) ligand 1 ( CXCL1 ), activating transcription factor 5 ( ATF5 ), and ATP/GTP binding protein‐like 2 ( AGBL2 ). Studies showed elevated CXCL1 is associated with tumor progression and poor prognosis in cancers; and the overexpression of ATF5 or AGBL2 enhances malignancy in cancer cells . The mechanisms of SRSF1 within different cellular compartments need to be further studied.…”