Roles of Interleukin-6 and Parathyroid Hormone-Related Peptide in Osteoclast Formation Associated with Oral Cancers

Kayamori, Kou; Sakamoto, Kei; Nakashima, Tomoki; Takayanagi, Hiroshi; Morita, Keiichi; Omura, Ken; Nguyen, Su Tien; Miki, Yoshio; Iimura, Tadahiro; Himeno, Akiko; Akashi, Takumi; Yamada-Okabe, Hisafumi; Ogata, Etsuro; Yamaguchi, Akira

doi:10.2353/ajpath.2010.090299

Cited by 68 publications

(74 citation statements)

References 45 publications

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“…Several oral SCC cells in patients and oral SCC cell lines express RANKL (38)(39)(40). Recently, Chuang et al compared RANKL expression between buccal SCC without bone invasion (25 cases) and gingival SCC with invasion (15 cases).…”

Section: Rankl/rank Signaling Is Involved In Oral Scc Cell-induced Osmentioning

confidence: 99%

The RANKL/RANK system as a therapeutic target for bone invasion by oral squamous cell carcinoma

Jimi

Shin

Furuta

et al. 2013

International Journal of Oncology

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Abstract. Squamous cell carcinomas (SCCs) of the gingiva frequently invade the mandible or maxilla; this invasion is associated with a worse prognosis. The bone destruction associated with carcinomal invasion is mediated by osteoclasts rather than directly by the carcinoma. Therefore, if the cellular and molecular mechanisms by which oral SCC regulates bone invasion were known, it could inform the development of new therapeutic targets. Recently, dysregulation of the functional equilibrium in the receptor activator of NF-κB ligand (RANKL)/RANK/osteoprotegerin (OPG) triad has been shown to be responsible for osteolysis associated with the development of malignant tumors in bone sites. Furthermore, the administration of OPG or soluble RANK prevents bone metastasis by cancer cells. In this review, we discuss recent findings indicating that bone invasion by oral SCC is mediated via RANKL/RANK and may be successfully prevented by RANKL inhibition.

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Section: Rankl/rank Signaling Is Involved In Oral Scc Cell-induced Osmentioning

confidence: 99%

The RANKL/RANK system as a therapeutic target for bone invasion by oral squamous cell carcinoma

Jimi

Shin

Furuta

et al. 2013

International Journal of Oncology

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“…The bidirectional tumor-stromal interaction often takes place at the TB interface where tumor cell-derived cytokines stimulate osteoclast differentiation, resulting in degradation of the bone matrix and the release of bone-derived cytokines that further promote tumor growth [1,26]. The activated factors at the TB interface implied the involvement of them in the tumor-stromal interaction [27,29,30]. We utilized a model of bone metastasis which was confirmed as a fine model to replicate the tumor-induced changes in bone microenvironment [31].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Bone Morphogenetic Proteins Type 1a Receptor (BMPR1a) in Breast Cancer Cells Protects Bone from Breast Cancer-Induced Osteolysis by Suppressing RANKL Expression

Yang

Zhang

Yuan

et al. 2018

Cell Physiol Biochem

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Key Words Bmpr1a • Breast cancer • Bone metastasis • Tumor-stromal interaction • Osteolysis • OsteoclastogenesisAbstract Background/Aims: Bone morphogenetic proteins (BMPs) and BMP receptors widely participate in osteolytic metastasis of breast cancer, while their role in tumor-stromal interaction is largely unknown. In this study, we investigated whether BMP receptor type 1a (BMPR1a) can alter the interaction between metastatic cancer cells and osteoclast precursors. Methods: Adenovirusmediated RNA interference was used to interrupt target genes of human breast cancer cell lines and nude mice were injected intratibially with the cancer cells. Tumor-bearing mice were examined by bioluminescence imaging and microCT. Sections of metastatic legs were measured by a series of staining methods. Murine bone marrow mononuclear cells or RAW264.7 cells were cultured with conditioned media of breast cancer cells. RT-PCR, Western blotting and ELISA were used to test mRNA and protein expressions of target molecules. Results: Expression of BMPR1a of MDA-MB-231-luc cells at tumor-bone interface was apparently stronger than that of cancer cells distant from the interface. Mice injected with BMPR1a-knockdown MDA-MB-231-luc cells showed reduced tumor growth and bone destruction compared with control groups. Knockdown (KD) of BMPR1a of MDA-MB-231-luc cells or MCF-7 cells decreased the level of receptor activator for NF-κB ligand (RANKL). Level of RANKL in MDA-MB-231-luc cells or MCF-7 cells was reduced by p38 inhibitor. Compared with control group, knockdown of p38 of breast cancer cells decreased cancer-induced osteoclastogenesis. Conclusion: Knockdown of BMPR1a of breast cancer cells suppresses their production of RANKL via p38 pathway and inhibits cancer-induced osteoclastogenesis, which indicates that BMPR1a might be a possible target in breast cancer-induced osteolytic metastasis.

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“…Many of studies showed that IHC plays an important role in pathology and particularly in the subspecialties of oncologic pathology , neuropathology and hematopathology , The first IHC study was reported at 1941 but the principle of immunohistochemistry has existed since the 1930s (Ajura et al .,2007). Kayamori et al (2010) were examined the expression of IL-6 to revealed that was this expression not only in cancer cells but also in fibroblasts and osteoclasts at the tumor bone interface. While, Becker et al (2005) were demonstrated that IL-6 can regulate the proliferation of intestinal epithelial cells (IEC) and inducing growth of dysplastic lesion in vivo as possible functional role of interleukin-6.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemistry Analysis for Interleukin-6 Expression from the Tumor Tissue

Suker¹,

Badran²,

Abbas³

et al. 2017

ijSciences

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Abstract:The cytokines including interleukins considered an important component of the body's immunity against inflammatory conditions and cancer diseases, and is an important factor in inducing the symptoms of wasting weight in cancer patients. Therefore, the knowledge and the study of these factors and their impact, production, particularly interleukin-6 gene expression and identification to recognize the presence and production of this factor in the tissues of patients through immunohistochemistry technique and gene expression. The study included 40 samples from different types of malignant tumor biopsy and (7) samples for benign tumor used as control. Immunohistochemistry (IHC) analysis revealed that there was an increase in the production of interleukin -6 which appeared as brown precipitate in the cytoplasm of cancer cell as positive staining , while, the benign tumor tissues (control ) showed negative staining.

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Roles of Interleukin-6 and Parathyroid Hormone-Related Peptide in Osteoclast Formation Associated with Oral Cancers

Cited by 68 publications

References 45 publications

The RANKL/RANK system as a therapeutic target for bone invasion by oral squamous cell carcinoma

The RANKL/RANK system as a therapeutic target for bone invasion by oral squamous cell carcinoma

Knockdown of Bone Morphogenetic Proteins Type 1a Receptor (BMPR1a) in Breast Cancer Cells Protects Bone from Breast Cancer-Induced Osteolysis by Suppressing RANKL Expression

Immunohistochemistry Analysis for Interleukin-6 Expression from the Tumor Tissue

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