CXCL5, the upregulated chemokine in patients with uterine cervix cancer, in vivo and in vitro contributes to oncogenic potential of Hela uterine cervix cancer cells

CXCL5/CXCR2 axis in tumor microenvironment as potential diagnostic biomarker and therapeutic target

“…CXCL5 has also been shown to be involved in many aspects of malignant progression of the tumor (Figure 2 and Table 2). CXCL5 promoted the proliferation of several types of tumor cells, such as the tumor cells in prostate cancer [54], cervical cancer [26], lung cancer [55], hepatoblastoma [56], and osteosarcoma [57]. The increasing expression of CXCL5 and IL-8 induced by snail also promoted prostate cancer cell growth in vivo by CXCR2 activation [58].…”

“…According to the previous studies, more than 14 different malignant tumor types, including breast cancer [15], bladder cancer [16], non-small cell lung cancer [17], gastric cancer [18], head and neck squamous cell carcinoma [19], cholangiocarcinoma [20], hepatocellular carcinoma [21], prostate cancer [22], pancreatic cancer [23], colorectal cancer [24], glioma [25], endometrial cancer [26], nasopharyngeal carcinoma [27], and squamous carcinoma of larynx [6], had high expression of CXCL5 when compared to para-carcinoma or normal tissues (Table 1). By identifying and validating the genes regarding the development of gastric cancer, researchers have found that CXCL5, as one of the substances, was associated with early stages of the disease [28].…”

“…Promote tumor angiogenesis and lymphangiogenesis in TME [51,52] Regulate the function of neutrophil in TME [45] Positively related to the risk of metastasis [62,63,72] Recruit immune cells -Recruit neutrophils in TME and metastatic niche [30,[42][43][44][45] -Recruit granulocytes to promote the formation of early metastatic microenvironment [40,49] -Promote MDSCs infiltration in TME [47,48] -Positively related to the extent of macrophage infiltration in TME [50] Promote cell proliferation of primary tumors [26,[54][55][56][57] Abbreviations: CXCL5, CXC motif ligand 5; TME, tumor microenvironment; MDSC, myeloid-derived suppressor cell.…”

CXCL3 overexpression promotes the tumorigenic potential of uterine cervical cancer cells via the MAPK/ERK pathway

“…In 40 UCC samples, the upregulated expression of CXCL3 was positively related to the UCC stage, but negatively related to other pathological parameters, including cancer infiltration and patient age (Table ), indicating a predominant effect for CXCL3 in the tumorigenesis of UCC. To fully elucidate the correlation of CXCL3 and CXCL5 expression, we performed a pathological correlation study using the present results on CXCL3 and our previous results on CXCL5 expression in UCC (Feng et al, ). The results demonstrated that CXCL3 expression was strongly concerned with CXCL5 expression in UCC tissues, and this correlation was closely associated with several pathological parameters, including clinical stage, tumor infiltration, and age (Table ).…”

“…In our previous investigation, we presented that exogenous CXCL5 and CXCL5 overexpressing facilitated the malignant behaviors of HeLa cells in vitro and in vivo in tumor xenografts (Feng et al, ). Since CXCL3 and CXCL5 share the same receptor, that is, CXCR2, we hypothesized that CXCR2‐mediated malignant processes in UCC may be partially modulated by another ligand of CXCL3.…”