Effect of TSLC1 gene on growth and apoptosis in human esophageal carcinoma Eca109 cells

Liang, Qiong; Wang, Bi-Rong; Li, Zhouyu; Chen, Guoqiang; Zhou, Yuan

doi:10.5114/aoms.2012.31251

Cited by 8 publications

(7 citation statements)

References 14 publications

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“…The cell adhesion molecule 1 (CADM1) gene, which is also known as TSLC1 or Necl-2 , has been generally investigated as a tumor-suppressor gene in various tumors, including prostate, esophageal, nasopharyngeal, non-small cell lung and cervical cancers ( 16 , 18 , 23 – 25 ). Many studies have shown that CADM1 , as a tumor-suppressor gene, is associated with inhibition of cell proliferation, as well as invasion and induction of apoptosis in various tumor cells, including the non-small cell lung cancer A549 cell line ( 26 ), human esophageal carcinoma Eca109 cells ( 27 ), and a hepatocellular carcinoma cell line ( 28 ). CADM1 is downregulated in many cancers, frequently via promoter hypermethylation ( 16 , 17 ).…”

Section: Discussionmentioning

confidence: 99%

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells

Woo

Kim

Song

et al. 2015

International Journal of Oncology

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Epigenetic modification at CpG islands located on the promoter regions of tumor-suppressor genes has been associated with tumor development in many human cancers. Our study showed that the cell adhesion molecule 1 (CADM1) is downregulated in human papillomavirus (HPV)-infected cervical cancer cell lines via its hypermethylation and demethylation using 5-aza-2′-deoxycyticine (5-aza-dC) restored the expression of CADM1 protein. Overexpression of CADM1 inhibited cell proliferation. p53 was involved in the regulation of CADM1. Our results demonstrate that epigenetic alteration of CADM1 was more frequent in HPV-positive cervical cancers and that restoration of CADM1 expression may be a potential strategy for cervical cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells

Woo

Kim

Song

et al. 2015

International Journal of Oncology

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“…Cell Adhesion Molecule 1 is a protein that has been found to be strongly expressed in neurons, [71][72][73][74][75] spermatogenic cells, [52,[76][77][78] immune cells, [79][80][81][82][83][84][85][86][87] and endothelial cells [88,89]. Functionally, CADM1 has been shown to participate in homophilic binding, and paradoxically, tumor suppression.…”

Section: Cadm1: An Additional Role For a Versatile Protein?mentioning

confidence: 99%

Tumor Necrosis Factor α Regulates Endothelial Progenitor Cell Migration via CADM1 and NF-kB

et al. 2016

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Shortly after the discovery of endothelial progenitor cells (EPCs) in 1997, many clinical trials were conducted using EPCs as a cellular based therapy with the goal of restoring damaged organ function by inducing growth of new blood vessels (angiogenesis). Results were disappointing, largely because the cellular and molecular mechanisms of EPC-induced angiogenesis were not clearly understood. Following injection, EPCs must migrate to the target tissue and engraft prior to induction of angiogenesis. In this study EPC migration was investigated in response to tumor necrosis factor α (TNFα), a pro-inflammatory cytokine, to test the hypothesis that organ damage observed in ischemic diseases induces an inflammatory signal that is important for EPC homing. In this study, EPC migration and incorporation were modeled in vitro using a co-culture assay where TNFα treated EPCs were tracked while migrating towards vessel-like structures. It was found that TNFα treatment of EPCs increased migration and incorporation into vessel-like structures. Using a combination of genomic and proteomic approaches, NF-kB mediated upregulation of CADM1 was identified as a mechanism of TNFα induced migration. Inhibition of NF-kB or CADM1 significantly decreased migration of EPCs in vitro suggesting a role for TNFα signaling in EPC homing during tissue repair.

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“…Although important advances exist in multimodal therapy of ESCC, prognosis remains poor, with a 5-year survival rate less than 15% [ 3 ]. Therefore, identifying reliable diagnostic and prognostic biomarkers of ESCC is critical, as well as elucidating molecular mechanisms participating in esophageal carcinogenesis [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

DEK overexpression is predictive of poor prognosis in esophageal squamous cell carcinoma

Duan

Shi

et al. 2021

Arch Med Sci

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Introduction: The DEK gene encodes a nuclear phosphoprotein which is involved in multiple cell metabolic processes, such as DNA damage repair, mRNA splicing, modifying chromatin structure and transcription regulation. DEK has been shown to be overexpressed in various solid human tumors and associated with patient prognosis. In this study, our aim was to investigate DEK protein expression and its relationship with clinicopathological parameters and prognosis in esophageal squamous cell carcinoma (ESCC). Material and methods: Tissue samples were collected from 120 routinely diagnosed ESCC patients who underwent surgical resection at the Zhongshan Hospital, Xiamen University in the period from June 2011 to May 2013. The expression of DEK was determined by immunohistochemistry. Results: DEK protein was ubiquitously distributed in the nucleus of ESCC cells, and its positive rate (71.7%) was significantly higher in cancer samples than those of para-carcinoma (21.4%) or normal esophageal (13.9%) tissues (p < 0.001). Similarly, significantly more cells overexpressing DEK were found in ESCC tissues (57.5%) in comparison with para-carcinoma samples (11.4%) and normal esophageal mucosa (0%, p < 0.001). The DEK overexpression rate was significantly different between patients with different tumor-node-metastasis (TNM) stages and differentiation degrees (p < 0.001). ESCC cases with elevated DEK amounts showed reduced disease-free and 5-year survival rates compared with those expressing low DEK amounts (p < 0.001). DEK overexpression was also confirmed to independently predict prognosis in ESCC (HR = 4.121, 95% CI: 1.803-9.42, p = 0.001). Conclusions: DEK expression is positively correlated with reduced survival in ESCC patients. DEK has potential to be an independent biomarker in predicting prognosis of ESCC patients.

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Effect of TSLC1 gene on growth and apoptosis in human esophageal carcinoma Eca109 cells

Cited by 8 publications

References 14 publications

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells

Tumor Necrosis Factor α Regulates Endothelial Progenitor Cell Migration via CADM1 and NF-kB

DEK overexpression is predictive of poor prognosis in esophageal squamous cell carcinoma

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