ADAR1: a promising new biomarker for esophageal squamous cell carcinoma?

Qiao, Jun; Chan, Tim; Qin, Yanru; Chen, Leilei

doi:10.1586/14737140.2014.928595

Cited by 15 publications

(10 citation statements)

References 38 publications

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“…In our previous study, we did not detect effects of 8-Cl-Ado on cell cycle profile and apoptosis in the cell lines. While in Stellrecht's study 24 ADAR1, a type of RNA-editing enzyme that catalyzes the adenosine into inosine on double-stranded RNA, is highly expressed in breast, lung, liver, and esophageal cancer, as well as in chronic myelogenous leukemia, where it promotes tumor progression depending on cancer types [17][18][19][20][21] . Previously, we showed that ADAR1 is increased in both breast cancer tissue samples and breast cancer cell line, especially, ADAR1-p110 isoform is dominantly expressed and promotes the proliferation and migration of breast cancer cells 7,8 .…”

Section: Discussionmentioning

confidence: 99%

8-Chloro-Adenosine Inhibits Proliferation of MDA-MB-231 and SK-BR-3 Breast Cancer Cells by Regulating ADAR1/p53 Signaling Pathway

et al. 2020

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8-Chloro-adenosine (8-Cl-Ado) has been shown to exhibit its antitumor activity by inducing apoptosis in human lung cancer A549 and H1299 cells or autophagy in chronic lymphocytic leukemia, and MDA-MB-231 and MCF-7 breast cancer cells. Adenosine deaminases acting on RNA 1 (ADAR1) is tightly associated with cancer development and progression. The aim of this study was to investigate the role of ADAR1 in the proliferation of MDA-MB-231 and SK-BR-3 breast cancer cell lines after 8-Cl-Ado exposure and its possible mechanisms. After 8-Cl-Ado exposure, CCK-8 assay was performed to determine the cell proliferation; flow cytometry was used to analyze the cell cycle profiles and apoptosis; and the protein levels of ADAR1, p53, p21, and cyclin D1 were measured by western blotting. The results showed that the cell proliferation was greatly inhibited, G1 cell cycle was arrested, and apoptosis was induced after 8-Cl-Ado exposure. ADAR1 and cyclin D1 protein levels were dramatically decreased, while p53 and p21 levels were increased after 8-Cl-Ado exposure. Moreover, the cell growth inhibition was rescued, apoptosis was reduced, and p53 and p21 protein levels were downregulated, while cyclin D1 was upregulated when cells were transfected with plasmids expressing ADAR1 proteins. More importantly, RNA-binding domain of ADAR1 is critical to the cell growth inhibition of breast cancer cells exposed to 8-Cl-Ado. Together, 8-Cl-Ado inhibits the cell proliferation, induces G1 phase arrest and apoptosis at least by targeting ADAR1/p53/p21 signaling pathway. The findings may provide us with insights into the role of ADAR1 in breast cancer progression and help us better understand the effects of 8-Cl-Ado in the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%

8-Chloro-Adenosine Inhibits Proliferation of MDA-MB-231 and SK-BR-3 Breast Cancer Cells by Regulating ADAR1/p53 Signaling Pathway

et al. 2020

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“…There are two major isoforms of ADAR1: An interferon-inducible ADAR1 p150 that contains both the Za and Zb Z-DNA-binding domains and a constitutive ADAR1 p110 that lacks the N-terminal Za Z-DNA-binding domain[35]. ADAR1 has emerged as a biomarker in numerous solid tumors, including gastric cancer and esophageal cancer[36,37]. In our study, StarBase 3.0 (http://starbase .sysu.edu.cn/index.php) was used, and ADAR1 was found to be co-expressed with MEG3 in CRC.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG3 acts a biomarker and regulates cell functions by targeting ADAR1 in colorectal cancer

Wang

Xie

Chen

et al. 2019

WJG

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BACKGROUND Colorectal cancer (CRC) is the third most prevalent malignancy and has the fourth highest global cancer mortality rate. Early diagnosis and prompt medical attention can improve quality of life and the prognosis of CRC patients. Accumulating evidence reveals that long non-coding RNAs (lncRNAs) function as oncogenes or anti-oncogenes, as well as biomarkers in various cancers. AIM To investigate the levels and molecular mechanism of the lncRNA maternally expressed gene 3 (MEG3) in CRC. METHODS The levels of lncRNA MEG3 in CRC tissue, serum and cell line samples were explored via qRT-PCR. The relationship between MEG3 levels and clinicopathological features in CRC was investigated. The diagnostic and prognostic values of serum MEG3 levels were analyzed with ROC curves and Kaplan‑Meier survival curves, respectively. RESULTS Significant decreased levels of MEG3 existed in CRC tissue, cell lines and serum. CRC patients with down-regulated serum MEG3 levels had larger tumor sizes, and advanced clinical stages. The sensitivity and specificity of serum MEG3 levels in CRC detection was 0.667 and 0.875, respectively. Tumor size, T stages, and serum MEG3 levels are indie factors that produce an effect on CRC patients' prognosis. Kaplan‑Meier survival curves suggested that CRC patients with high levels of MEG3 had a remarkably better overall survival rate. CONCLUSION LncRNA MEG3 is down-regulated in CRC, and regulates cell functions by targeting adenosine deaminase’s effect on RNA 1 in CRC.

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“…Recently, numerous studies aimed to explore early predictive markers for early diagnosis of ESCC. Adenosine deaminase acting on RNA 1 ( ADAR1 ), significantly overexpressed in ESCC, was reported as a potential biomarker of ESCC diagnosis and prognosis and as a new molecular therapeutic target [ 17 ]. Wang et al .…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, targeting SOX9 by either small interfering RNAs (siRNAs) or microRNAs significantly reduced tumor cell proliferation and invasion, chondrogenic differentiation in human mesenchymal stem cells, or resistance to targeted therapy for lung adenocarcinoma [ 14 – 16 ]. SOX9 is also overexpressed in ovarian cancer and it could be a possible diagnostic marker of ovarian carcinomas [ 17 ]. Collectively, these studies indicate that SOX9 functions as an oncogene and might represent an anti-cancer target.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of sex-determining region Y-box 9 (SOX9) promotes cell proliferation and tumorigenicity in esophageal squamous cell carcinoma

Yun

Chen

et al. 2015

Oncotarget

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Sex-determining region Y-box 9 (SOX9), a vital transcription factor, play important roles in numerous biological and pathological processes. However, the clinical significance and biological role of SOX9 expression has not been characterized in human esophageal squamous cell cancer (ESCC). Herein, we found that SOX9 was markedly upregulated, at both mRNA and protein level, in ESCC cell lines and ESCC tissues and that SOX9 expression was significantly correlated with tumor clinical stage, T classification, N classification, M classification, pathological differentiation, and shorter overall survival. The proliferation and tumorigenicity of ESCC cells were dramatically induced by SOX9 overexpression but were inhibited by SOX9 knockdown both in vitro and in vivo. Moreover, we demonstrated that upregulation of SOX9 increased the expression of phosphorylated Akt, the cyclin-dependent kinase (CDK) regulator cyclin D1, phosphorylated forkhead box O (FOXO)1, and phosphorylated FOXO3, but SOX9 downregulation decreased their expression, whereas the levels of the CDK inhibitors p21Cip1 and p27Kip1 were attenuated in SOX9-transduced cells. Taken together, our results suggest that SOX9 plays an important role in promoting the proliferation and tumorigenesis of ESCC and may represent a novel prognostic marker for the disease.

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ADAR1: a promising new biomarker for esophageal squamous cell carcinoma?

Cited by 15 publications

References 38 publications

8-Chloro-Adenosine Inhibits Proliferation of MDA-MB-231 and SK-BR-3 Breast Cancer Cells by Regulating ADAR1/p53 Signaling Pathway

8-Chloro-Adenosine Inhibits Proliferation of MDA-MB-231 and SK-BR-3 Breast Cancer Cells by Regulating ADAR1/p53 Signaling Pathway

LncRNA MEG3 acts a biomarker and regulates cell functions by targeting ADAR1 in colorectal cancer

Upregulation of sex-determining region Y-box 9 (SOX9) promotes cell proliferation and tumorigenicity in esophageal squamous cell carcinoma

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