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Roles as Potential Oncogene or tumour suppressor of the Midclustered MicroRNAs in Gallid Herpesvirus 2(GaHV2)-Induced Marek's Disease Lymphomagenesis

Roles as Potential Oncogene or Tumour Suppressor of the Midc...

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第九届全国核糖核酸学术讨论会

作者： Man Teng Zu-Hua Yu Pu Zhao Zi-Xiang Wu Lu Dang Hui-Zhen Li Sheng-Ming Ma Gai-Ping Zhang 罗俊河南省农业科学院 College of Animal Science and Veterinary Medicine Henan Agricultural University

In the last decade,numerous of miRNAs have been identified in diverse virus families,particularly in *** herpesvirus2(Ga HV2)is a representativeoncogenic alphaherpesvirus that induces rapid-onset T-cell lymphomas in its natural hosts namely Marek’s disease(MD).In Ga HV2 genome,the presence of26 mature miRNAs derived from 14 precursors assembled in three clusters,namely Meq-cluster,Mid-cluster and LAT-cluster,*** Ga HV2 miRNAs,especially for those in Meq-cluster(***-M4),have been demonstrated to be critical for MD pathogenesis and/or *** downstream Mid-cluster is regulated and transcribed by a same promoter of Meq-cluster,but the role of Mid-clustered miRNAs in Ga HV2 biology remains ***,we have generated Mid-cluster and associated individual miRNA deletion mutants in GX0101 virus,a very virulent(vv)Ga HV2 *** Ga HV2-infected chickens as animal models,we found that deletion of Mid-cluster significantly increased viral pathogenicity as *** to parental GX0101 virus,the individual deletion of miR-M1 and miR-M11separately increased the viral pathogenicity or oncogenecity while the individual deletion of miR-M31 significantly decreased the mortality and gross tumour incidence of virus infected ***,our data confirms that in Ga HV2 infection,the viral oncogene meq is targeted and down-regulated by miR-M11-5p,a miR-M11-derived mature *** the best of our knowledge,this is the first report to present that the Mid-clustered miRNAs possibly act either as potential oncogene or tumour suppressor in MD lymphomagenesis.

关键词： Herpesvirus GaHV2 miRNA oncogene tumour suppressor

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MicroRNAs, development of Barrett’s esophagus, and progression to esophageal adenocarcinoma

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World Journal of Gastroenterology 2010年第5期16卷 531-537页

作者： Cameron M Smith David I Watson Michael Z Michael Damian J Hussey Department of Surgery Flinders University Room 3D211 Flinders Medical Centre Bedford Park South Australia 5042 Australia Department of Gastroenterology & Hepatology Flinders University Bedford Park South Australia 5042 Australia

Barrett's esophagus is a premalignant condition caused by gastroesophageal reflux. Once developed, it can progress through varying grades of dysplasia to esoph-ageal adenocarcinoma. Whilst it is well accepted that Barrett's esophagus is caused by gastroesophageal reflux, the molecular mechanisms of its pathogenesis and progression to cancer remain unclear. MicroRNAs (miRNAs) are short segments of RNA that have been shown to control the expression of many human genes. They have been implicated in most cellular processes, and the role of miRNAs in disease development is be-coming increasingly evident. Understanding altered miRNA expression is likely to help unravel the molecular mechanisms that underpin the development of Barrett's esophagus and its progression to cancer.

关键词： Barrett’s esophagus MicroRNA Esophageal adenocarcinoma Transdifferentiation tumour suppressor

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Csk-homologous kinase （Chk/Matk）： a molecular policeman suppressing cancer formation and progression

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Frontiers in Biology 2015年第3期10卷 195-202页

作者： Gahana Advani Anderly C. Chueh Ya Chee Lim Amardeep Dhillon Heung-Chin Cheng Department of Biochemistry and Molecular Biology Bio21 Molecular Science and Biotechnology Institute University of Melbourne 30 Flemington Road Parkville Victoria 3010 Australia A CRF Chemical Biology Division The Walter and Eliza Hall Institute for Medical Research Royal Melbourne Hospital and Department of Medical Biology University of Melbourne Parkville Victoria 3052 Australia Peter MacCallum Cancer Research Institute St. Andrews Place East Melbourne Hctoria Australia

Aberrant activation of Src-family tyrosine kinases （SFKs） directs initiation of metastasis and development of drug resistance in multiple solid tumors and hematological cancers. Since oncogenic mutations of SFKs are rare events, aberrant activation of SFKs in cancer is likely due to dysregulation of the two major upstream inhibitors： C-terminal Src kinase （Csk） and its homolog Csk-homologous kinase （Chk/Matk）. Csk and Chk/Matk inhibit SFKs by selectively phosphorylating the inhibitory tyrosine residue at their C-terminal tail. Additionally, Chk/Matk can also employ a non- catalytic inhibitory mechanism to inhibit multiple active forms of SFKs, suggesting that Chk/Matk is a versatile inhibitor capable of constraining the activity of multiple active forms of SFKs. Mounting evidence suggests that Chk/ Mark is a potential tumor suppressor downregulated by epigenetic silencing and/or missense mutations in several cancers such as colorectal and lung carcinoma. In spite of the potential significance of Chk/Matk in cancer, little is known about its structure and regulation. This review focuses on the mechanisms by which Chk/Matk expression and activity is downregulated in cancers. Specifically, we assessed the evidence demonstrating downregulation of Chk/Matk by epigenetic silencing and missense mutations in cancers. The other focus is the tumor suppressive mechanism of Chk/ Matk. The final focus of the review is on the clinical applications of the investigations into the mechanism of epigenetic silencing of Chk/Matk expression and the tumor suppressive mechanism of Chk/Matk; specifically we discussed how they can benefit the development of biomarkers for early diagnosis of cancers and specific SFK inhibitors for use as cancer therapeutics.

关键词： tumour suppressor protein tyrosine kinase Src-family kinases CSK CHK/Matk colon cancer

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Aberrant Expression of Notch1 in Cervical Cancer

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Chinese Journal of Clinical Oncology 2007年第1期4卷 38-41页

作者： Li Sun Qimin Zhan Wenhua Zhang Yongmei Song Tong Tong Department of Gynecological Oncology Cancer Hospital and Institute Chinese Academy of Medical Sciences Beijing 100021 China State Key Laboratory of Molecular Oncology Cancer Hospital and Institute Chinese Academy of Medical Sciences Beijing 100021 .China

OBJECTIVE To investigate the putative role of the Notch1 receptor in cervical cancer carcinogenesis and progression. METHODS The expression of the Notch1 protein was analyzed by a Western-blotting approach in 40 cervical cancer and 30 normal cervical tissues. Some tissues were examined using RT-PCR to determine mRNA levels. Celluar localization of the Notch1 protein in the paraffin-embedded cervical tissues was also analyzed by immunohistochemistry. RESULTS The Notch1 protein was detected in all 30 normal cervical tissues. In contrast, only 6 samples of 40 cervical cancer tissues showed Notch1 expression. The level of the Notch1 protein expression was significantly lower in cervical cancer tissues than that in normal tissue samples. In agreement with these observations, levels of Notch1 mRNA were found to be substantially down-regulated in cervical cancer tissues. In the immunohistochemistry staining assay, the Notch1 protein was shown to localize predominantly in the cytoplasm and nucleoli of the normal cervical squamous epithelium of the cervix, but no staining was observed in the cervical cancer cells. Notch1 expression was observed to correlate with the clinical disease stage, but there were no correlations with age, tumor size, grade or lymph node metastasis （P〉0.05）. The levels of Notch1 protein expression were significantly higher in early stages （Ⅰ-Ⅱa, 66.7%） compared to those in the advanced stages （Ⅱb～Ⅳ,12.6%）（P=0.001）. CONCLUSION Notch1 may play a role as a tumor suppressor in cervical tumorigenesis. Determination of Notch1 expression may be helpful for preoperative diagnosis and accuracy of staging. But its clinical use for cervical cancer requires further investigation.

关键词： cervical cancer tumour suppressor Notch1.

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