Identification and Characterization of Microrna-135a in Cervical Carcinogenesis
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Home > Medicine & Health Science textbooks > Medical specialties, branches of medicine > Gynaecology and obstetrics > Identification and Characterization of Microrna-135a in Cervical Carcinogenesis
Identification and Characterization of Microrna-135a in Cervical Carcinogenesis

Identification and Characterization of Microrna-135a in Cervical Carcinogenesis


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About the Book

This dissertation, "Identification and Characterization of MicroRNA-135A in Cervical Carcinogenesis" by Oi-ning, Leung, 梁靄嬣, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Cervical cancer is the second major cancer among women worldwide and is associated with persistent infection of human papillomaviruses (HPVs). However, exposure to high-risk type HPVs alone is insufficient for tumor formation. Additional factors are required for the HPV-infected cervical cells to become tumorigenic. Activation of -catenin/TCF signaling is essential for transformation of HPV-immortalized keratinocyte into cancer. -catenin is excessively expressed in cervical cancer. Dysregulation of microRNAs is profoundly observed in various cancers but their roles in cervical cancer are obscure. MicroRNA-135a (miR-135a) regulates one of the negative regulators of -catenin signaling, E3 ubiquitin ligase Seven In Absentia Human Homolog 1 (SIAH1). A 39-fold increase in the expression of miR-135a occurs in early stage cervical cancer. This study hypothesized that over-expression of miR-135a transformed HPV-infected cervical cells to cancer by activating -catenin/TCF signaling through down-regulation of SIAH1. In this study, miR-135a was confirmed to be specifically up-regulated in cervical cancer tissues when compared with precancerous lesions. Force-expression of miR-135a induced tumorigenic properties (anchorage independent growth and metastatic abilities) in vitro of a non-tumorigenic cervical epithelial cell line NC104 immortalized by HPV-16 E6 and E7 oncoproteins (NC104 E6/E7). The metastatic activities induced by miR-135a required the presence of E6 and E7 proteins as the activities were not observed in another immortalized cervical cell-line from the same parental cells but without the oncoproteins. The observations were confirmed by the observations that miR-135a knockdown did not impair the above tumorigenic properties in a HPV-negative cervical cancer cell line, but suppressed them in HPV-positive cervical cancer cell lines. The mechanism of action of miR-135a in cervical cancer was evaluated. The tumorigenic effects was due to the inhibitory action of miR-135a on SIAH1 leading to up-regulation of -catenin/TCF signaling. MiR-135a force-expression enhanced the growth of the cervical cancer cell line HeLa and NC104 E6/E7-derived tumor in vivo. The effect of miR-135a was partially nullified by SIAH1 force-expression. These observations were in line with expression analyses in cervical biopsies, in which SIAH1 immunoreactivities were inversely correlated, whereas -catenin was positively correlated with the expression of miR-135a. The data illustrated an oncogenic role of miR-135a/SIAH1/-catenin signaling in cervical cancer formation. The role of miR-135a in the formation of cancer stem cells (CSCs) was also elucidated. The number of CD133+ cells was significantly higher in the miR-135a-transformed NC104 E6/E7 cells than the untreated group. The CD133+ cells isolated from the miR-135a-transformed NC104 E6/E7 possessed self-renewal, differentiation and multidrug resistance properties, up-regulation of miR-135a. They also expressed -catenin and the stemness genes OCT4, SSEA-4. CD133+ cells were also identified sporadically in fresh cervical tumors. The observations indicate that CD133+ cervical cancer cells possesses CSC properties. In conclusion, this thesis was the first to identify and characterize the functions of miR-135a as an oncomiR in cervical carcinogenesis. MiR-135a played a pivotal role in malignant transformation and cance


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Product Details
  • ISBN-13: 9781361344644
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 294
  • Weight: 685 gr
  • ISBN-10: 1361344644
  • Publisher Date: 27 Jan 2017
  • Binding: Paperback
  • Language: English
  • Spine Width: 16 mm
  • Width: 216 mm


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