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  • The endothelin receptor type B EDNRB belongs to the family

    2021-05-14

    The endothelin receptor type B (EDNRB) belongs to the family of G protein-coupled receptors, which functions as a vital regulatory factor in signal transduction in cells, locating on human chromosome 13q22.3 (Ayala-Valdovinos et al., 2016; Bregar et al., 2018; Morimoto et al., 2018; Widowati et al., 2016). It has been confirmed that EDNRB exhibited high level of methylation and reduced expression of mRNA in tumors like nasopharyngeal cancer (Lo et al., 2002; Xu et al., 2016; Zhou et al., 2007), esophageal squamous cell carcinoma (Zhao et al., 2009), oral squamous cell carcinoma (Viet et al., 2011), leukemia (Hsiao et al., 2008), gastric cancer (Tao et al., 2012) and colorectal cancer (Chen et al., 2013; Mousavi Ardehaie et al., 2017). Furthermore, EDNRB also participated in the initiation and development of malignant tumors. Mou et al. found that the mRNA expression and protein level of EDNRB were downregulated in hepatoma cell line and HCC tissues, which could inhibit the metastasis and invasion of HCC BAY 11-7082 SMMC-7721 and Huh7 (Mu, 2017). Nonetheless, further researches are required in the clinical significance of EDNRB and molecular mechanism in HCC.
    Materials and methods
    Results
    Discussion The endothelin receptor type B (EDNRB), a member of the G protein-coupled receptors, was located on human chromosome 13q22.3 (Ayala-Valdovinos et al., 2016; Bregar et al., 2018; Lo et al., 2002; Zhang and Sui, 2014). Previous studies demonstrated that the abnormal methylation of EDNRB and its aberrant expression of mRNA were detected in various malignancies, and also EDNRB was found to participate in the onset and development of malignant tumors (Chen et al., 2013; Mousavi Ardehaie et al., 2017; Schussel et al., 2013; Xu et al., 2016). For instance, in the nasopharyngeal cancer, Lo et al. discovered the higher methylation of EDNRB in the tumor tissues rather than in normal nasopharynx tissues (Lo et al., 2002). Zhou et al. also confirmed that higher level of methylation was observed in the tissues of nasopharyngeal cancer than in the tissues of chronic nasopharyngitis, and the downregulated expression of EDNRB was detected in the tissues of nasopharyngeal carcinoma and the nasopharyngeal carcinoma cell line (Zhou et al., 2007).In esophageal squamous cell carcinoma, Zhao et al. found that the mRNA of EDNRB was more remarkably lowly expressed in tumor tissues than in normal controls; in addition, increased EDNRB methylation was detected in tumor tissues (Zhao et al., 2009). In oral squamous cell carcinoma, Viet et al. suggested that high methylation of EDNRB was associated with the pain caused by the cancer (Viet et al., 2011). Hsiao et al. demonstrated that patients with leukemia tended to have the highly methylated EDNRB promoter (Hsiao et al., 2008).In gastric cancer, the result of Tao et al. showed that the increased methylation of EDNRB was closely related with the infiltration and metastasis of the gastric carcinoma, indicating that EDNRB might play a vital part in the pathogenesis of the gastric cancer (Tao et al., 2012). In colorectal cancer, research by Chen et al. suggested that the highly methylated promoter of EDNRB downregulated the its mRNA expression and took part in the initiation and progression of the colorectal carcinoma (Chen et al., 2013). Besides, Mousavi et al. confirmed that the aberrant methylation of EDNRB could be used as the potential diagnostic marker of the colorectal cancer (Mousavi Ardehaie et al., 2017). Despite the abovementioned studies, we researchers were still BAY 11-7082 less informed of the clinical significance of EDNRB in HCC and the molecular mechanism.
    Funding This study was supported by the Open Fund of Guangxi Colleges and Universities Key Laboratory of Biological Molecular Medicine Research (Grant number: GXBMR201601), National Natural Science Foundation of China (Grant number: NSFC81560386), funds of Guangxi Zhuang Autonomous Region Health, Family Planning Commission Self-Financed Scientific Research Project (Grant number: Z20170556), the Key Programs of Natural Science Foundation of Guangxi, China (Grant number: 2017GXNSFAA198107, 2015GXNSFDA139028), and the Key Programs of University Scientific Research of Guangxi Education Agency (Grant number: ZD2014033).