A preliminary study of the effect of ECRG4 overexpression on the proliferation and apoptosis of human laryngeal cancer cells and the underlying mechanisms

Jia, Jianping; Song, Dae‐Kyu; Sun, Xiaoyang; Sang, Yue-Hong; Xu, Zhonghua; Zhang, Jie; Cui, Xiaofeng; Song, Jinhui; Guo, Xing

doi:10.3892/mmr.2015.4059

Cited by 20 publications

(13 citation statements)

References 31 publications

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“…Overexpression of ECRG4 induced cell cycle arrest in G1 phase and then suppressed the proliferation of GC cells, which is consistent with previous studies. 17 , 18 In addition, Jia et al have revealed that ECRG4 is associated not only with proliferation but also with apoptosis. 17 In laryngeal cancer, overexpression of ECRG4 induced apoptosis by regulating the expression of apoptosis-related factors, such as Bax, Bcl-2, and caspase-3.…”

Section: Discussionmentioning

confidence: 99%

“… 17 , 18 In addition, Jia et al have revealed that ECRG4 is associated not only with proliferation but also with apoptosis. 17 In laryngeal cancer, overexpression of ECRG4 induced apoptosis by regulating the expression of apoptosis-related factors, such as Bax, Bcl-2, and caspase-3. ECRG4 could also play a role in anti-inflammatory activities by interacting with an immunity receptor complex, which might be important for tumor immunity.…”

Section: Discussionmentioning

confidence: 99%

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Downregulation and DNA methylation of ECRG4 in gastric cancer

Deng¹,

Chang²,

Gao³

et al. 2018

OTT

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BackgroundEsophageal cancer-related gene 4 (ECRG4) is a novel candidate tumor suppressor gene. Our study investigated the expression and function of ECRG4 in gastric cancer and highlighted the role of DNA hypermethylation at the promoter in silencing the ECRG4 expression.MethodsThe GSE63089 data set was obtained from the Gene Expression Omnibus and analyzed for differentially expressed genes. Carcinoma and para-carcinoma tissues of 102 patients with gastric cancer were collected from January 2010 to July 2011. Immunohistochemistry, real-time polymerase chain reaction (PCR), and western blot analyses were performed to evaluate the expression of ECRG4. After measuring the change in the level of ECRG4 expression, CCK-8, Transwell, and flow cytometric cell cycle assays were performed. In addition, methylation-specific PCR was performed to detect the methylation state of ECRG4, and 5-aza-2′-deoxycytidine was used for demethylation of ECRG4. All statistical analyses were performed using the SPSS 17.0 software.ResultsWe found that ECRG4 expression was downregulated in gastric cancer, and this was closely related to lymph node metastasis. After ECRG4 was silenced using a specific small interfering RNA, the BGC-823 cell line became highly aggressive and proliferative. In addition, we verified whether downregulation of ECRG4 was highly correlated with DNA methylation of the ECRG4 promoter and found that the demethylating agent 5-aza-2′-deoxycytidine could effectively enhance ECRG4 expression.ConclusionThe aberrant expression of ECRG4 is associated with hypermethylation in the promoter region and plays an important role in the malignancy of gastric cancer. Therefore, ECRG4 may be a potential biomarker for molecular diagnosis of gastric cancer, and the use of 5-Aza-dC to reverse the hypermethylation of ECRG4 may be a new approach to the treatment of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Downregulation and DNA methylation of ECRG4 in gastric cancer

Deng¹,

Chang²,

Gao³

et al. 2018

OTT

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“…An example is the C-Myc proto-oncogene which is the X-linked XIAP inhibitor of apoptosis protein and Caspase-3 apoptotic promotion factor [24]. Caspase-3 is called the death protease because it is a critical executive protease whose activation leads inevitably to apoptosis [25,26]. The C-Myc transcription factor is found constitutively expressed in many cancers; including lung, stomach, breast and colon cancer and also in cervical carcinoma [27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Over-expression of MEOX2 promotes apoptosis through inhibiting the PI3K/Akt pathway in laryngeal cancer cells

Tian

Tao

et al. 2018

neo

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The early-stage diagnosis and treatment for the recurrence of larynx carcinoma needs further investigation. Mesenchyme homeobox 2 (MEOX2) was speculated as a novel suppressor gene in larynx carcinoma in our study, the molecular mechanism was studied. Real-time quantitative PCR (RT-qPCR) and Western blot were used to detect mRNA and protein levels of MEOX2 in laryngeal cancer tissues and cells (Hep-2, TU212, AMC-NH-8 and TU686 cells), and also apoptosis and phosphoinositide 3-kinase (PI3K)/protein kinase (Akt) related factors in TU212 cells transfected with MEOX2. Cell counting kit-8 (CCK8) assay and Annexin-Ⅴ/PI staining assay were conducted to determine cell viability and apoptosis rates respectively.46 patients with larynx carcinoma were involved in this study. The expression of MEOX2 was lower in larynx carcinoma tissues than normal tissues, correlated with clinical stages, differentiated degrees, and survival times. The expression of MEOX2 was the lowest among those laryngeal cancer cells, and was chosen to be transfected with MEOX2 in the following study. Over-expression of MEOX2 inhibited cell viability and promoted apoptosis of TU212 cells, via increasing the expression levels of Caspase-3, and decreasing levels of C-Myc, XIAP, PI3K p110α, PI3K p110β, PI3K class III and p-Akt. In summary, the expression levels of MEOX2 were inhibited in larynx carcinoma than normal tissues, correlated with the progression of the cancer. Over-expression of MEOX2 in laryngeal cancer cells inhibited cell viability and promoted apoptosis, via regulating apoptosis and PI3K/Akt pathway related factors. It would provide evidence for MEOX2 to be used as a therapeutical gene in larynx carcinoma.

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“…Thereafter, more studies demonstrated that ECRG4 was involved in the initiation and progression of numerous types of cancer, including breast carcinoma, squamous cell carcinoma of the head and neck, gastric cancer and neurogliocytoma ( 6 , 18 – 20 ). In particular, low ECRG4 expression level was reported to significantly promote tumor cell migration and inhibit apoptosis ( 9 , 17 , 21 ). The present study investigated ECRG4 expression level in HCC.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of esophageal cancer-related gene 4 promotes proliferation and migration of hepatocellular carcinoma

Wang

et al. 2017

Oncology Letters

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Esophageal cancer-related gene 4 (ECRG4) is a candidate tumor suppressor gene, which is involved in cell apoptosis, migration, infection and inflammation responsiveness; however, its expression level and clinical significance in hepatocellular carcinoma (HCC) remains unclear. In the present study, the authors aim to evaluate the clinical significance and potential role of ECRG4 in HCC. Level of ECRG4 protein expression in HCC and peripheral tissues was investigated in tissue specimens obtained from 56 consecutive HCC patients by immunohistochemistry. Cell proliferation, cell migration and invasion regulations were examined by MTT curves, flow cytometry, Transwell assays and western blotting. ECRG4 expression was weak positive in normal liver cells but was downregulated in HCC cells in vivo or in vitro. A decreased expression of ECRG4 was associated with the age of the patients, metastasis and Ki-67 proliferation index. However, decreased ECRG4 expression was not associated with differentiation, tumor size, the presence of portal vein tumor thrombosis, satellite lesions, tumor relapse or mortality. Further investigations revealed that ectopic expression of ECRG4 inhibited cell proliferation, migration and invasion and promoted cell apoptosis in SMMC-7721 cells, which was mediated by the regulation of BAX and B cell lymphoma-2, in addition to the upregulation of epithelial-mesenchymal transition markers. In conclusion, the results of the present study indicated that ECRG4 was downregulated in HCC and served important roles in promoting cell proliferation and migration.

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A preliminary study of the effect of ECRG4 overexpression on the proliferation and apoptosis of human laryngeal cancer cells and the underlying mechanisms

Cited by 20 publications

References 31 publications

Downregulation and DNA methylation of ECRG4 in gastric cancer

Downregulation and DNA methylation of ECRG4 in gastric cancer

Over-expression of MEOX2 promotes apoptosis through inhibiting the PI3K/Akt pathway in laryngeal cancer cells

Downregulation of esophageal cancer-related gene 4 promotes proliferation and migration of hepatocellular carcinoma

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