Induction of apoptosis in human salivary gland tumor cells by anti-NCAM antibody

Fukuda, Masakatsu; Horiuchi, Yuko; Oku, Yuka; Ishikawa, Marin; Suka, Noriyuki; Suzuki, Seiji; Kusama, Kaoru; Sakashita, Hideaki

doi:10.3892/or.14.5.1143

Cited by 7 publications

(14 citation statements)

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“…Furthermore, it has been described that NCAM is expressed by a variety of human tumors and associated with perineural invasion by various neoplasms, such as gallbladder cancer, melanoma, bile duct cancer, and adenoid cystic carcinoma of the head and neck [30][31][32][33][34][35]. We have also demonstrated previously that NCAM is sporadically found in the adenoid cystic carcinoma, derived from human submandibular salivary gland, in vivo [36]. NCAM is believed to mediate adhesion between cells through a calcium ion-independent homophilic (NCAM-NCAM) binding mechanism and to mediate adhesion between neurons and the extracellular matrix through heterophilic binding (NCAM to another ligand or counter-receptor) [21].…”

Section: Neural Cell Adhesion Molecule (Ncam)supporting

confidence: 72%

The Mechanisms of Proliferation and Energy Metabolism in Oral Cancer

Fukuda¹,

Sakashita²

2019

Prevention, Detection and Management of Oral Cancer

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Human oral squamous cell carcinoma (HOSCC) is the most common head and neck malignant neoplasm. Therapy is generally performed in multidisciplinary approach that used chemotherapy, radiotherapy, and surgery against patients with oral cancer; however, we cannot avoid dysfunction due to its side effects or surgical defects, and it significantly impacts the postoperative quality of life, unfortunately. Therefore, a better understanding of the molecular mechanisms driving oral carcinogenesis may lead to new diagnostic and therapeutic approaches to this disease and improve the prognosis of HOSCC patients. Cancer cells process a fundamental change in its bioenergetics metabolism from normal cells on an altered glucose and lipid metabolism. Recent insights into tumor metabolism have further revealed that oncogenic signaling pathways directly promote metabolic reprogramming to upregulate biosynthesis of lipids, carbohydrates, protein, DNA, and RNA, leading to enhanced growth of tumors. Therefore, targeting cell metabolism has become a novel direction for drug development in oncology. Moreover, molecular mechanisms causing these metabolic changes are just starting to be unraveled. This chapter presents recent findings on molecular markers that have been involved in the mechanisms of proliferation and energy metabolism of oral cancer and in addition provides new perspectives on oral cancer diagnosis and treatments.

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Section: Neural Cell Adhesion Molecule (Ncam)supporting

confidence: 72%

The Mechanisms of Proliferation and Energy Metabolism in Oral Cancer

Fukuda¹,

Sakashita²

2019

Prevention, Detection and Management of Oral Cancer

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“…These amounts were loaded per lane and separated on a polyacrylamide gel of appropriate percentage, then the proteins were electroblotted onto nitrocellulose membranes. Subsequent immunoblot analysis was carried out according to the method reported previously (22).…”

Section: Enzyme-linked Immunosorbent Assay (Elisa)mentioning

confidence: 99%

“…Total RNA was extracted from monolayer HOSCC cells (1x10 6 cells/ml) by the acid-guanidinium-phenol-chloroform (AGPC) method reported previously (22). To confirm the expression patterns of up-regulated or down-regulated IL-23 and RelA genes in HOSCC cells, especially HSC-3 cells, derived from metastatic lymph node of tongue cancer, treated with or without TNF-· (10 ng/ml), IL-23 (10 ng/ml), or IL-23 (10 ng/ml) + PAb IL23p19 (0.8 μg/ml), real-time quantitative RT-PCR analyses were performed using a Bio-Rad iCycler system (Bio-Rad, Tokyo, Japan) and an iScript One-Step RT-PCR kit with SYBR Green I (Bio-Rad) according to the manufacturer's instructions.…”

Section: Rna Extraction and Real-time Quantitative Rt-pcrmentioning

confidence: 99%

IL-23 promotes growth and proliferation in human squamous cell carcinoma of the oral cavity

Fukuda

M²,

Suzuki³

et al. 2010

Int J Oncol

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Abstract. Interleukin (IL)-23 is a heterodimeric cytokine, comprising IL-12p40 and the cloned IL-23-specific p19 subunit, was identified as a cancer-associated cytokine in a recent study. Like IL-12, IL-23 is expressed predominantly by activated dendritic cells and phagocytic cells. These cytokines antagonistically regulate local inflammatory responses in the tumor microenvironment and infiltration by intraepithelial lymphocytes. We have previously demonstrated the expression of IL-23 and its receptors in human oral squamous cell carcinoma (HOSCC) cell lines and tissue. Hence, this study investigated whether IL-23 has a role in the growth and proliferation of oral cancer cells by examining the expression kinetics of IL-23 and NF-κB activity, in vitro and in vivo. IL-23, which constitutively expressed in oral cancer, was enhanced by TNF-· and IL-23. IL-23 promotes cell proliferation in oral cancer and enhances the transport of nuclear factor-κB (NF-κB p65, RelA) to the nucleus in HSC-3 cells. Furthermore, luciferase reporter assay showed that IL-23 strongly induces RelA activity, and confirmed this finding by knockdown of IL-23 using RNA interference. Although RelA activity was down-regulated by anti-human IL-23p19 polyclonal antibody, used to neutralize the activity of IL-23, apoptosis was not induced. Immunohistochemistry revealed a weak IL-23 immunoreactivity in the cytoplasm of inflammatory infiltrating cells and in the cancer cells derived from 14 of 40 cases (35%) of oral SCC. In contrast, strong RelA immunoreactivity was observed in 30 of 40 cases of SCC (75%), especially consistent with IL-23 positive cells in SCC tissues. These data suggest that IL-23 up-regulates the growth and cell proliferation of oral cancer by promoting the nuclear transactivation of RelA.

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“…Total rna was extracted from monolayer HoScc cells (1x10 6 cells/ml) by a previously reported acid-guanidinium-phenol-chloroform (aGPc) method (14). To confirm the expression of IL-23p19, IL-23R and il-12rβ1 genes, rT-Pcr analysis was performed.…”

Section: Rna Extraction and Rt-pcrmentioning

confidence: 99%

Section: Rna Extraction and Rt-pcrmentioning

confidence: 99%

Expression of interleukin-23 and its receptors in human squamous cell carcinoma of the oral cavity

Fukuda¹

2009

Mol Med Rep

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Abstract. interleukin (il)-23 is a heterodimeric cytokine comprising IL-12p40 and the recently cloned IL-23-specific p19 subunit. like il-12, il-23 is expressed predominantly by activated dendritic cells and phagocytic cells. Both cytokines induce interferon-γ secretion by T cells, and antagonistically regulate local inflammatory responses in the tumor microenvironment as well as the infiltration of intraepithelial lymphocytes. although the expression of il-23 in various organs has been reported, it is unclear whether il-23 is expressed in oral cancer. The expression of il-23 and its receptors was examined in human oral squamous cell carcinoma (HoScc) cell lines and tissue. il-23 and its receptor mrnas and proteins were spontaneously expressed, and il-23 was increased by TnF-α stimulation in the oral cancer cells. A cell proliferation assay confirmed that IL-23 promotes cell proliferation in oral cancer. The localization of il-23 protein in HoScc tissue was examined using immunohistochemistry. a positive reaction for anti-il-23 antibody was weakly observed in the cytoplasm of inflammatory infiltrating cells and cancer cells in HoScc tissue. Meanwhile, nuclear factor-κB immunoreactivity was strongly positive in HoScc tissue, which is particularly consistent with the observation of il-23-positive cells in Scc tissue. These data suggest that IL-23 plays a significant role in the growth and proliferation of oral cancer.

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Induction of apoptosis in human salivary gland tumor cells by anti-NCAM antibody

Cited by 7 publications

References 0 publications

The Mechanisms of Proliferation and Energy Metabolism in Oral Cancer

The Mechanisms of Proliferation and Energy Metabolism in Oral Cancer

IL-23 promotes growth and proliferation in human squamous cell carcinoma of the oral cavity

Expression of interleukin-23 and its receptors in human squamous cell carcinoma of the oral cavity

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