CSF3 contributes to the invasive and metastatic phenotypes and associates with poor prognosis in patients with colorectal cancer via NF-κB signaling pathway

Abstract

Abstract Background Colony-stimulating factor 3 (CSF3) is a cytokine associated with inflammation, which mainly stimulates myeloid stem cell maturation, proliferation, and migration into circulation. However, the significance of CSF3 in colorectal cancer (CRC) remains unclear. Here, we aimed to examine the expression and impacts of CSF3 in CRC. Methods CSF3 expression was examined in CRC tissues and cells by IHC staining and western blot. RNA interference was used to silence CSF3 in CRC cells. The effects of CSF3 on biological behaviors such as proliferation and migration of CRC cells were examined in vitro and in vivo. Results CSF3 was highly expressed in CRC tissues and cells. CSF3 high level was correlated to patients’ age, with a feature of a higher pathological stage, more distant lymphatic metastasis and more severe lymph node invasion. Knocking down CSF3 led to decreased proliferation and migration, increased apoptosis, arrested cell cycle in vitro as well as impaired tumor growth in vivo. Mechanistically, CSF3 regulates CRC cell proliferation and apoptosis dependent on enhances p65 phosphorylation to facilitate NF-κB-mediated transcriptional activity. Conclusion Our study demonstrated that CSF3 interacts with the NF-κB signaling pathway to promote the progression of CRC. CSF3 might be a potential therapeutic target for CRC patients.