Expression of MIP-3α/CCL20, a macrophage inflammatory protein in oral squamous cell carcinoma

doi:10.1016/S0003-9969(02)00167-X

Archives of Oral Biology

Volume 48, Issue 2, February 2003, Pages 171-175

https://doi.org/10.1016/S0003-9969(02)00167-X Get rights and content

Abstract

We have examined the expression of MIP-3α/CCL20 in oral squamous cell carcinoma (SCC) in vivo and in vitro. In addition, we have investigated whether the expression of MIP-3α/CCL20 is regulated by bacterial infection and inflammatory cytokines. In order to determine the mRNA level of MIP-3α, quantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed with LightCycler™ using the double-stranded DNA dye, SYBR Green I. Oral epithelial cells and six SCC cell lines (SCC-9, SAS, BSC-OF, HSC-4, HSC, Ca9-22) were found to express MIP-3α mRNA. The expression of MIP-3α was upregulated by infection with Actinobacillus actinomycetemcomitans and by stimulation with lipopolysaccharide and TNF-α. By in situ hybridization, the detectable MIP-3α expression in SCC was localized primarily at the epithelial pearls corresponding to the spinous layer. These results suggest that MIP-3α contributes to the oral immunoresponse to bacterial infection, and may be involved in the growth of SCC.

Section snippets

Acknowledgements

We thank Ms. R. Yagami for her excellent technical assistance.

References (17)

K. Hieshima et al.
Molecular cloning of a novel human CC chemokine liver and activation-regulated chemokine (LARC) expressed in liver
J. Biol. Chem.
(1997)
R. Hromas et al.
Cloning and characterization of EXODUS, a novel b-chemokine
Blood
(1997)
A. Zlotnik et al.
Chemokines: a new classification system and their role in immunity
Immunity
(2000)
Y. Abiko et al.
Pattern of expression of beta-defensins in oral sqamous cell carcinoma
Cancer Lett.
(1999)
Y. Tanaka et al.
Selective expression of liver and activation-regulated chemokine (LARC) in intestinal epithelium in mice and humans
Eur. J. Immunol.
(1999)
A.-S. Charbonnier et al.
Macrophage inflammatory protein 3α is involved in the constitutive trafficking of epidermal Langerhans cells
J. Exp. Med.
(1999)
J. Bancherau et al.
Dendritic cells and the control of immunity
Nature
(1998)
D.L. Rossi et al.
Identification through bioinflammatory human chemokines. MIP-3α and MIP-3b
J. Immunol.
(1997)

There are more references available in the full text version of this article.

Cited by (43)

Targeting anticancer immunity in oral cancer: Drugs, products, and nanoparticles
2023, Environmental Research
Oral cavity carcinomas are the most frequent malignancies among head and neck malignancies. Oral tumors include not only oral cancer cells with different potency and stemness but also consist of diverse cells, containing anticancer immune cells, stromal and also immunosuppressive cells that influence the immune system reactions. The infiltrated T and natural killer (NK) cells are the substantial tumor-suppressive immune compartments in the tumor. The infiltration of these cells has substantial impacts on the response of tumors to immunotherapy, chemotherapy, and radiotherapy. Nevertheless, cancer cells, stromal cells, and some other compartments like regulatory T cells (Tregs), macrophages, and myeloid-derived suppressor cells (MDSCs) can repress the immune responses against malignant cells. Boosting anticancer immunity by inducing the immune system or repressing the tumor-promoting cells is one of the intriguing approaches for the eradication of malignant cells such as oral cancers. This review aims to concentrate on the secretions and interactions in the oral tumor immune microenvironment. We review targeting tumor stroma, immune system and immunosuppressive interactions in oral tumors. This review will also focus on therapeutic targets and therapeutic agents such as nanoparticles and products with anti-tumor potency that can boost anticancer immunity in oral tumors. We also explain possible future perspectives including delivery of various cells, natural products and drugs by nanoparticles for boosting anticancer immunity in oral tumors.
Role of chemokines in HPV-induced cancers
2022, Seminars in Cancer Biology
Human papillomaviruses (HPVs) cause cancers of the uterine cervix, oropharynx, anus, and vulvovaginal tract. Low-risk HPVs, such as HPV6 and 11, can also cause benign mucosal lesions including genital warts, and in patients with recurrent respiratory papillomatosis, lesions in the larynx, and on occasion, in the lungs. However, both high and less tumorigenic HPVs share a striking commonality in manipulating both innate and adaptive immune responses in HPV- infected keratinocytes, the natural host for HPV infection. In addition, immune/inflammatory cell infiltration into the tumor microenvironment influences cancer growth and prognosis, and this process is tightly regulated by different chemokines. Chemokines are small proteins and exert their biological effects by binding with G protein‐coupled chemokine receptors (GPCRs) that are found on the surfaces of select target cells. Chemokines are not only involved in the establishment of a pro-tumorigenic microenvironment and organ-directed metastases but also involved in disease progression through enhancing tumor cell growth and proliferation. Therefore, having a solid grasp on chemokines and immune checkpoint modulators can help in the treatment of these cancers. In this review, we discuss the recent advances on the expression patterns and regulation of the main chemokines found in HPV-induced cancers, and their effects on both immune and non-immune cells in these lesions. Importantly, we also present the current knowledge of therapeutic interventions on the expression of specific chemokine and their receptors that have been shown to influence the development and progression of HPV-induced cancers.
Significance of chemokine and chemokine receptors in head and neck squamous cell carcinoma: A critical review
2016, Oral Oncology
Chemokines are small chemotactic proteins that coordinate circulation of immune/inflammatory cells throughout body compartments. Because of this property chemokines and their cell surface receptors are implicated in several physiological and pathological conditions, including cancer. These molecules are expressed by neoplastic or stromal cells and have effects at tumor primary site (e.g. stimulating angiogenesis and tumor cells motility) and lymph nodes (creating a gradient to direct migration of neoplastic cells). In this article we review the current knowledge about the function(s) of chemokines and receptors in squamous cell carcinoma from the oral cavity and head and neck region. Accumulating evidence suggests some chemokine(s) and receptor(s) as potential targets in adjuvant therapies for these malignancies.
Expression profiles for 14-3-3 zeta and CCL20 in pancreatic cancer and chronic pancreatitis
2014, Pathology Research and Practice
Pancreatic cancer (PCA) has a dismal prognosis because it is often diagnosed at an advanced stage. The overall survival rate is <5% after five years. Chronic pancreatitis (CP) is one of the most important risk factors for PCA. A major difficulty is to distinguish between CP and PCA at both clinical and morphologic level. The aim of this study was to assess the impact of the expression profiles for 14-3-3 zeta and CCL20 to histologically discriminate between PCA and CP.
In PCA (n = 138) and CP (n = 36) tissue samples, the expression of 14-3-3 zeta and CCL20 was examined by immunohistochemistry. Associations between expression profiles of 14-3-3 zeta and CCL20 expression in PCA, CP as well as MANT (matched adjacent normal tissue) (n = 138) and clinicopathologic variables were analyzed.
The expression of CCL20 and 14-3-3 zeta was significantly higher in PCA than in CP and MANT. For CP compared to MANT, no significant differences were observed for expression profiles of both 14-3-3 zeta and CCL20.
CCL20 and 14-3-3 zeta are molecules that play a putative role during tumorgenesis in pancreas, and may therefore be new parameters for histological diagnosis and discrimination between PCA and CP.
Expression profile of drosomycin-like defensin in oral epithelium and oral carcinoma cell lines
2013, Archives of Oral Biology
Drosomycin-like defensin (DLD) is a recently discovered antimicrobial peptide mainly active against filamentous fungi. The present study investigated the expression profile of DLD in oral epithelium and oral squamous cell carcinoma (SCC) cell lines.
Tissue sections of human oral mucosa, keratinocytes derived from oral mucosa (NOK) and eight kinds of SCC cell lines were used. In situ hybridization was performed on tissue sections of oral mucosa. Expression levels of DLD in the cells were observed by reverse transcription polymerase chain reaction (RT-PCR) and real-time RT-PCR assays. The cells were treated with IL-1β, IL-8 and TNF-α, and agonists for TLR2, TLR4 and β-glucan. DLD expression in cells was increased and decreased by the DLD gene and its siRNA transfection, respectively. The proliferation rates were assessed by cell counting.
By means of in situ hybridization, DLD mRNA positive staining was detected in the epithelial layer of the oral mucosa. An RT-PCR assay confirmed the expression of DLD mRNA in keratinocytes derived from oral epithelium. Expression of DLD in two out of eight cell lines was significantly lower than in NOK cells. The expression levels of DLD mRNA were not significantly changed in the cells stimulated with any cytokines or agonists. The cell proliferation rate where there was decreased expression of DLD was significantly lower than in the control.
DLD may be partially involved in the defence against filamentous fungal infection in the oral mucosa, and may also serve other functions, such as contribution to cell growth.
High Expression of CCL20 Is Associated with Poor Prognosis in Patients with Hepatocellular Carcinoma after Curative Resection
2012, Journal of Gastrointestinal Surgery
Chemokine ligand 20 (CCL20) plays an important role in the carcinogenesis, invasion, and progression of malignancies. This study aimed to investigate the prognostic significance of CCL20 in patients with hepatocellular carcinoma (HCC) after curative resection.
Expression of CCL20 was evaluated by immunohistochemistry in tumor tissue from 125 patients who underwent curative resection of HCC. The relationship between CCL20 expression and clinicopathologic features was analyzed. Univariate and multivariate analyses were performed to evaluate its predictive value for tumor recurrence and survival of HCC patients.
CCL20 expression was verified in all tumor specimens. CCL20 expression was associated with tumor size (P = 0.002), tumor number (P = 0.031), vascular invasion (P = 0.003), tumor differentiation (P = 0.024), and tumor recurrence (P < 0.001). Patients with high CCL20 expression had poorer recurrence-free survival and overall survival (both P < 0.001) than those with low CCL20 expression. Multivariate analysis showed CCL20 expression was an independent predictor of tumor recurrence (Hazard ratio 3.934, P = 0.002), recurrence-free survival (Hazard ratio 2.573, P = 0.001), and overall survival (Hazard ratio 2.930, P = 0.001).
CCL20 expression was associated with tumor recurrence and survival of HCC patients. It may be used to predict prognosis of patients with HCC and may be a new target of postoperative adjuvant therapy.

View all citing articles on Scopus

View full text

SHORT COMMUNICATIONExpression of MIP-3α/CCL20, a macrophage inflammatory protein in oral squamous cell carcinoma

Abstract

Section snippets

Acknowledgements

J. Biol. Chem.

Blood

Immunity

Cancer Lett.

Selective expression of liver and activation-regulated chemokine (LARC) in intestinal epithelium in mice and humans

Eur. J. Immunol.

Macrophage inflammatory protein 3α is involved in the constitutive trafficking of epidermal Langerhans cells

J. Exp. Med.

Dendritic cells and the control of immunity

Nature

Identification through bioinflammatory human chemokines. MIP-3α and MIP-3b

J. Immunol.

SHORT COMMUNICATION
Expression of MIP-3α/CCL20, a macrophage inflammatory protein in oral squamous cell carcinoma