CT120A Acts as an Oncogene in Head and Neck Squamous Cell Carcinoma

Baltaci, Elif; Ekizoglu, Seda; Sarı, Elif; Karaman, Emin; Ulutin, Turgut; Buyru, Nur

doi:10.7150/jca.12969

Cited by 5 publications

(6 citation statements)

References 15 publications

(30 reference statements)

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“…Until recently CT120 had been associated only with lung cancer 3 - 5 . In our previous report we have shown that CT120 acts as an oncogene in HNSCC 6 . Depending on our previous data we hypothesized that CT120 may have important functions in the progression of HNSCC needing further investigation.…”

Section: Discussionmentioning

confidence: 87%

“…These results indicate that CT120 may be a key modulator in lung carcinogenesis and might contribute to the activation of oncogenic pathways in human lung cancer cells. In a previous study we have observed that the CT120A isoform is overexpressed also in head and neck squamous cell carcinoma (HNSCC) tumors 6 . However, no detailed information is available on the structural features of the CT120 gene.…”

Section: Introductionmentioning

confidence: 98%

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CT120: A New Potential Target for c-Myc in Head and Neck Cancers

et al. 2017

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Background: CT120 is a universally expressed protein with seven transmembrane domains. It functions in cell proliferation, survival and apoptosis by activating Raf/MEK/ERK and PI3K/Akt signaling pathways. Evidence suggests that CT120 plays important roles in lung carcinogenesis and oncogenic pathway activation. c-Myc is an important transcription factor modulating cell progression, apoptosis and cellular transformation. Previous studies have shown that MYC gene is amplified in many types of cancer including head and neck squamous cell carcinoma (HNSCC). Myc can regulate expression of many genes by binding to E-boxes. The aim of this study was to investigate the relationship between c-Myc protein and CT120 gene.Methods: Tumor and normal tissue samples from 50 patients with HNSCC were investigated with chromatin immunoprecipitation assay (ChIP), Illumina MiSeq, bisulphite sequencing and qRT-PCR.Results: c-Myc binds to all E-boxes except E-box 5 on CT120 promoter. The CpG dinucleotides were found to be partially methylated in all tumor and normal tissue samples. Bisulphite sequencing showed a 10% down-regulation in the methylation levels of the tumor tissues. CT120 gene was hypomethylated and up-regulated in 56% of the tumor tissue samples. Expression of c-Myc was significantly higher in tumor tissues than in non-cancerous tissue samples. MYC was overexpressed in 68% of the tumor tissue samples compared to normal tissues. The mean MYC levels were 2.42-fold higher in the tumor tissue samples. In 48% of the tumor tissues, MYC and CT120A mRNA were up- or down-regulated simultaneously (p<0.001).Conclusion: We show that CT120 gene is a target of c-Myc and it contributes to cancer progression in HNSCC.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 98%

CT120: A New Potential Target for c-Myc in Head and Neck Cancers

et al. 2017

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“…FAM57A has also been linked to human carcinogenesis and both pro- and anti-tumorigenic activities have been described. For lung, liver, and head and neck cancers, FAM57A expression was reported to be increased in tumors compared to the corresponding normal tissues [ 10 , 11 , 12 , 13 , 14 ]. Interference with FAM57A expression in cell lines derived from lung and liver cancers acted anti-proliferative [ 12 , 13 , 14 ], suggesting a pro-tumorigenic role for FAM57A in these tumor entities.…”

Section: Introductionmentioning

confidence: 99%

FAM57A (Family with Sequence Similarity 57 Member A) Is a Cell-Density-Regulated Protein and Promotes the Proliferation and Migration of Cervical Cancer Cells

Yang

Strobel

Bulkescher

et al. 2022

Cells

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The FAM57A (family with sequence similarity 57 member A) gene is controversially discussed to possess pro- or anti-tumorigenic potential. Here, we analyze the regulation of cellular FAM57A protein levels and study the functional role of FAM57A in HPV-positive cervical cancer cells. We find that FAM57A protein expression strongly depends on cell density, with FAM57A being readily detectable at low cell density, but undetectable at high cell density. This regulation occurs post-transcriptionally and is not mirrored by corresponding changes at the RNA level. We further show that FAM57A protein levels are highly increased in cervical cancer cells cultivated at hypoxia compared to normoxia and provide evidence that FAM57A is a hypoxia-responsive gene under control of the α-subunit of the HIF-1 (hypoxia-inducible factor-1) transcription factor. Yet, the strong relative increase of FAM57A protein levels in hypoxic cells is predominantly cell-density-dependent and occurs post-transcriptionally. Other anti-proliferative effectors besides hypoxia, such as silencing of HPV E6/E7 oncogene expression in cervical cancer cells, also result in an increase of FAM57A levels compared to untreated cells. Functional analyses reveal that FAM57A repression leads to pronounced anti-proliferative as well as anti-migratory effects in cervical cancer cells. Taken together, these results provide insights into the regulation of FAM57A protein levels and reveal that they underlie a tight cell-density-dependent control. Moreover, they identify FAM57A as a critical determinant for the phenotype of cervical cancer cells, which promotes their proliferation and migration capacities.

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“…A study in India reported the mutation in Rat sarcoma (Ras) gene is related to the development and progression of OSCC (Saranath et al, 1991). A more recent study reported CT120A gene as possible oncogene for HNSCC and its overexpression is associated with high tumor grades (Baltaci et al, 2015).…”

Section: Introduction and Epidemiology Of Head And Neck Cancermentioning

confidence: 99%

Head and neck cancer management and cancer stem cells implication

Elkashty

Ashry

2019

The Saudi Dental Journal

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Head and neck squamous cell carcinomas (HNSCCs) arise in the mucosal linings of the upper aerodigestive tract and are heterogeneous in nature. Risk factors for HNSCCs are smoking, excessive alcohol consumption, and the human papilloma virus. Conventional treatments are surgery, radiotherapy, chemotherapy, or a combined modality; however, no international standard mode of therapy exists. In contrast to the conventional model of clonal evolution in tumor development, there is a newly proposed theory based on the activity of cancer stem cells (CSCs) as the model for carcinogenesis. This “CSC hypothesis” may explain the high mortality rate, low response to treatments, and tendency to develop multiple tumors for HNSCC patients. We review current knowledge on HNSCC etiology and treatment, with a focus on CSCs, including their origins, identifications, and effects on therapeutic options.

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CT120A Acts as an Oncogene in Head and Neck Squamous Cell Carcinoma

Cited by 5 publications

References 15 publications

CT120: A New Potential Target for c-Myc in Head and Neck Cancers

CT120: A New Potential Target for c-Myc in Head and Neck Cancers

FAM57A (Family with Sequence Similarity 57 Member A) Is a Cell-Density-Regulated Protein and Promotes the Proliferation and Migration of Cervical Cancer Cells

Head and neck cancer management and cancer stem cells implication

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