Relationship of Angiogenesis and Oral Squamous Cell Carcinoma

Marla, Vinay; Hegde, Vibha; Shrestha, Ashish

doi:10.3126/kumj.v13i2.16796

Cited by 9 publications

(8 citation statements)

References 32 publications

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“…The most important prognostic indicator for patients with oral squamous cell carcinoma (OSCC) is metastasis to cervical lymph nodes or distant organs [1].The process of metastasis consists of sequential and selective steps including proliferation, induction of angiogenesis, detachment, motility, invasion into circulation, aggregation and survival in the circulation, cell arrest in distant capillary beds, and extravasation into organ parenchyma [2]. The development of a metastasis depends on interplay between host factors and intrinsic characteristics of cancer cells, and the metastatic lesion represents the end point of many destructive events that only a few cells can survive [3,4].…”

Section: Introductionmentioning

confidence: 99%

Targeting of Survivin Pathways by YM155 Inhibits Cell Death and Invasion in Oral Squamous Cell Carcinoma Cells

Zhang

Liu

et al. 2016

Cell Physiol Biochem

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Background/Aims: Specific overexpression in cancer cells and evidence of oncogenic functions make Survivin an attractive target in cancer therapy. The small molecule compound YM155 has been described as the first “Survivin suppressant” but molecular mechanisms involved in its biological activity and its clinical potential remain obscure. Survivin protein plays critical roles in oral squamous cell carcinoma (OSCC), suggesting that YM155 would be extremely valuable for OSCC. In this study, we tested our hypothesis whether YM155 could be an effective inhibitor of cell growth, invasion and angiogenesis in oral squamous cell carcinoma (OSCC) cells. Methods: SCC9 and SCC25 were treated with different concentration of YM155 for indicated time. Using MTT assay and flow cytometry analysis to detect cell growth and apoptosis; Using transwell and Wound healing assay to detect migration and invasion; Using reverse transcription-PCR, Western blotting and electrophoretic mobility shift assay for measuring gene and protein expression, and DNA binding activity of NF-κB. Results: YM155 inhibited survivin-rich expressed SCC9 cell growth in a dose- and time dependent manner. This was accompanied by increased apoptosis and concomitant attenuation of NF-κB and downregulation of NF-κB downstream genes MMP-9, resulting in the inhibition of SCC9 cell migration and invasion in vitro and caused antitumor activity and anti metastasis in vivo. YM155 treatment did not affect cell growth, apoptosis and invasion of surviving-poor expressed SCC25 cells in vitro. Conclusions: YM155 is a potent inhibitor of progression of SCC9 cells, which could be due to attenuation of survivin signaling processes. Our findings provide evidence showing that YM155 could act as a small molecule survivin inhibitor on survivin-rich expressed SCC9 cells in culture as well as when grown as tumor in a xenograft model. We also suggest that survivin could be further developed as a potential therapeutic agent for the treatment of survivin-rich expressed OSCC.

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Section: Introductionmentioning

confidence: 99%

Targeting of Survivin Pathways by YM155 Inhibits Cell Death and Invasion in Oral Squamous Cell Carcinoma Cells

Zhang

Liu

et al. 2016

Cell Physiol Biochem

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“…Angiogenesis is a complex process that is essential for the growth of cancer [ 30 ]. Therefore, in this paper we detected angiogenesis factors expression as VEGF and eNOS.…”

Section: Resultsmentioning

confidence: 99%

Beneficial effect of KYP-2047, a propyl-oligopeptidase inhibitor, on oral squamous cell carcinoma

et al. 2021

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Oral squamous cell-carcinoma (OSCC) is a common cancer which arises from the alveolar ridge, buccal mucosa, and tongue. Among OSCC, the incidence of tongue squamous cell-carcinoma (TSCC) is growing all over the world. Oral carcinogenesis has been linked to genetic mutations, chromosomal aberrations and viral factors. Apoptosis and angiogenesis play a key role in the development of oral cancer. Therefore, it is very important discover new therapeutic strategies to counteract oral cancer progression. This study aimed to investigate the effect of KYP-2047 in an in vitro model of TSCC and in vivo CAL27-xenograft model. Our results demonstrated that KYP-2047 was able to reduce TSCCs cell viability at the concentrations of 50 µM and 100 µM. Additionally, KYP-2047 was able to increase Bax, Bad and caspase-3 expression, whereas Bcl-2 and p53 expression were reduced. Moreover, KYP-2047 significantly reduced vascular-endothelial-growth-factor (VEGF) and endothelialnitric-oxide-synthase (eNOS) expression. In the vivo xenograft model, KYP-2047 at doses of 1 and 5 mg/kg significantly reduced tumor burden and tumor weight, decreasing also angiogenesis markers VEGF and eNOS. Moreover, KYP-2047 increased Bax and reduced Bcl2 expressions. Thus, KYP-2047 could represent a potential therapeutic treatment to counteract tongue oral-cancer growth, thanks its abilities to modulate angiogenesis and apoptosis pathways.

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“…Angiogenesis is essential for the development of OSCC [ 29 ]. Understanding the underlying mechanisms of OSCC angiogenesis may assist with the development of novel treatment approaches for OSCC, which has a low overall 5-year survival rate, despite improvements in surgical management and therapeutic combinations of radiation and chemotherapy [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

The Chemokine CCL4 Stimulates Angiopoietin-2 Expression and Angiogenesis via the MEK/ERK/STAT3 Pathway in Oral Squamous Cell Carcinoma

Tsai

Yang

et al. 2022

Biomedicines

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Oral squamous cell carcinoma (OSCC) is a common malignant tumor with a poor prognosis and is a major public health burden in Taiwan. Angiogenesis, the formation of new blood vessels, promotes tumor proliferation, maintenance, and metastasis. Angiopoietin 2 (Angpt2), a mitogen with a strong angiogenic effect, is highly specific to endothelial cells and a key player in angiogenesis. The inflammatory chemokine (C-C motif) ligand 4 (CCL4) is also important in the pathogenesis and progression of cancer. In this study, an analysis of records from The Cancer Genome Atlas (TCGA) database found higher CCL4 expression in oral cancer tissue than in normal healthy tissue. CCL4 treatment of oral cancer cells upregulated Angpt2 expression and stimulated mitogen-activated protein kinase kinase (MEK), extracellular signal-regulated kinase 1/2 (ERK), and signal transducer and activator of transcription 3 (STAT3) phosphorylation. Transfection of oral cancer cells with MEK, ERK, and STAT3 inhibitors and their small interfering RNAs inhibited CCL4-induced promotion of Angpt2 expression and angiogenesis. In a mouse model of OSCC, CCL4-treated cells promoted neovascularization in implanted Matrigel plugs, whereas inhibiting CCL4 expression suppressed Angpt2 expression and angiogenesis. CCL4 shows promise as a new molecular therapeutic target for inhibiting angiogenesis and metastasis in OSCC.

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Relationship of Angiogenesis and Oral Squamous Cell Carcinoma

Cited by 9 publications

References 32 publications

Targeting of Survivin Pathways by YM155 Inhibits Cell Death and Invasion in Oral Squamous Cell Carcinoma Cells

Targeting of Survivin Pathways by YM155 Inhibits Cell Death and Invasion in Oral Squamous Cell Carcinoma Cells

Beneficial effect of KYP-2047, a propyl-oligopeptidase inhibitor, on oral squamous cell carcinoma

The Chemokine CCL4 Stimulates Angiopoietin-2 Expression and Angiogenesis via the MEK/ERK/STAT3 Pathway in Oral Squamous Cell Carcinoma

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