CXCL5 overexpression is associated with late stage gastric cancer

Park, Jeong Youp; Park, Kyung Hwa; Bang, Seungmin; Kim, Myoung-Hwan; Lee, Ji Eun; Gang, Jingu; Koh, Sang Seok; Song, Si Young

doi:10.1007/s00432-007-0225-x

Cited by 88 publications

(73 citation statements)

References 35 publications

(32 reference statements)

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“…Previous studies have shown that overexpression of CXCL5 is present in numerous human tumors including prostate, squamous cell and stomach tumors. Additionally, CXCL5 may have an important role in the occurrence and progression of tumors by cooperating with its receptor C-X-C chemokine receptor type 2 (CXCR2) (14)(15)(16). Although a previous study by Zhou et al (17) demonstrated that the expression of CXCL5 in hepatocellular carcinoma tissues was evidently increased compared with that in para-carcinoma tissues and overexpression of CXCL5 can promote the growth and invasion of hepatocellular carcinoma cells, the effects of CXCL5 contributing to the growth and migration of HB cells through the autocrine/paracrine pathways have not, to the best of our knowledge, been reported.…”

Section: Introductionmentioning

confidence: 99%

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

et al. 2017

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Abstract. C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma. IntroductionHepatoblastoma (HB) is a prevalent malignancy among children, which histologically derives from pluripotent stem cells that may differentiate into liver cells and biliary epithelial cells, and accounts for almost two-thirds of pediatric malignant liver tumors (1,2). Although the survival rate of HB has increased from 35 to 75% during the last 30 years with the application of surgical excision, adjuvant chemotherapy and liver transplantation (3), additional investigation of the underlying molecular mechanism will be beneficial for the improving diagnosis and treatment of patients with HB.Previous studies have supported the hypothesis that the development of malignancies is closely associated with various cytokines, in which chemokines appear to have crucial roles. Chemokines are members of the cytokine super family and are secreted by various cell types, including immune, mesothelial, endometrial glandular and stromal cells, and trophoblasts (4). According to the order of conserved cysteine residues, chemokines are classified as C, CC, CXC and C (X) 3 C. Additionally, CXC chemokines are further grouped into ELR + CXC and ELR -CXC on the b...

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Section: Introductionmentioning

confidence: 99%

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

et al. 2017

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“…It has been reported that CXCL5 expression contributes to tumor progression and metastasis (30)(31)(32). Park et al demonstrated that CXCL5 overexpression was associated with advanced gastric cancer and high N stage, suggesting a role for CXCL5 in the progression of gastric cancer, specifically in lymph node metastasis (33).…”

Section: Introductionmentioning

confidence: 99%

CD44v6, MMP-7 and nuclear Cdx2 are significant biomarkers for prediction of lymph node metastasis in primary gastric cancer

Okayama

Kumamoto²,

Saitou³

et al. 2009

Oncol Rep

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Abstract. The aim of this study was to examine the expression of CD44v6, CD54, Cdx2, CXCL5, Cyclin B1, MMP-7, nm23, RCAS1 and Survivin in primary gastric cancer and to investigate whether these molecules were useful in predicting the lymph node status. They were selected as candidates for indicators of lymph node metastasis from various kinds of cancer-associated genes reported previously. In 135 cases of radically resected primary gastric adenocarcinoma, we investigated the association between the expression of these molecules and clinocopathologic factors by immunohistochemistry. The results revealed that the expression of CD44v6 and MMP-7 were significantly associated with lymph node status. By contrast, nuclear Cdx2 expression was found to be inversely correlated with lymph node metastasis. Moreover, multivariate analysis demonstrated that CD44v6, MMP-7 and nuclear Cdx2 were independent predictors for lymph node status. In conclusion, our results suggest that positive expression of both CD44v6 and MMP-7, and negative expression of nuclear Cdx2 may serve as powerful predictors of lymph node metastasis in gastric cancer. Combined evaluation of these markers could be further useful to predict lymph node status clinically.

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“…Moreover, a meta-analysis carried out by Liu et al [135] indicated that the variable results reported by many different studies can be affected by differences of histological type, tumor location, H. pylori infection, ethnicity and geographic location [136] . Another CXC chemokine, CXCL5, was also reported recently to be a potential molecular marker for cancer development, especially for late stage gastric cancer [137] . However, it is not yet confirmed if this observation is a consequence of secondary change as a result of gastric cancer progression, or whether it is one of the primary molecular events leading to tumor development.…”

Section: Stomachmentioning

confidence: 97%

“…Marker for late stage gastric cancer [137] Other candidates CC-chemokines (CCL2, 3, 5, 21, 25)/CXC-chemokines (1,7,8,12,14)/CCR6 [139] Liver CXCR4 Metastasis, upregulation in PVTT [142][143] …”

Section: Cxcl5mentioning

confidence: 99%

Chemokines, chemokine receptors and the gastrointestinal system

Miyazaki¹,

Takabe²,

Yeudall³

2013

WJG

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Core tip: The chemokine network makes an attractive target for therapeutic intervention in many tumor types, including those of the gastrointestinal tract. However, we need to define more selective and specific targets, to minimize systemic side effects during treatment. INTRODUCTION Cancer development and progression in the gastrointestinal tractCancer is a disease in which normal cells acquire genetic and epigenetic abnormalities [1,2] , leading to disorientation of conventional processes for the maintenance of normal cell physiology. These aberrant genetic and epigenetic modifications to the normal cell induce abnormal cell motility, proliferation, and survival, eventually enabling these cells to invade into adjacent tissues and even to migrate to regional or distant organs where they may grow continuously as metastatic lesions [3] . For many cancer patients, metastasis is generally the major cause of disease-related death [4,5] . Therefore, it is indispensable to elucidate the basic molecular mechanisms of tumor development to identify effective therapeutic targets, which can possibly reduce the side-effects of treatment, and define useful molecular markers for early detection and prediction of disease course. Especially, the newly emerged concept of personalized medicine may require in-depth assessment of potential therapeutic molecular target(s) in each individual case through analysis of sig- REVIEW Chemokines, chemokine receptors and the gastrointestinal system AbstractThe biological properties of tumor cells are known to be regulated by a multitude of cytokines and growth factors, which include epidermal growth factor receptor agonists and members of the transforming growth factor β family. Furthermore, the recent explosion of research in the field of chemokine function as mediators of tumor progression has led to the possibility that these small, immunomodulatory proteins also play key roles in carcinogenesis and may, therefore, be potential targets for novel therapeutic approaches. In this review, we will summarize recently reported findings in chemokine biology with a focus on the gastrointestinal tract.

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CXCL5 overexpression is associated with late stage gastric cancer

Abstract: CXCL5 overexpression was associated with late stage gastric cancer and high N stage. These results suggest a role for CXCL5 in the progression of gastric cancer, specifically in lymph node metastasis.

Cited by 88 publications

References 35 publications

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

CXCL5 as an autocrine or paracrine cytokine is associated with proliferation and migration of hepatoblastoma HepG2 cells

CD44v6, MMP-7 and nuclear Cdx2 are significant biomarkers for prediction of lymph node metastasis in primary gastric cancer

Chemokines, chemokine receptors and the gastrointestinal system

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