| Summary: | 碩士 === 國立陽明大學 === 口腔生物研究所 === 105 === Abstract
Oral carcinoma (OC) is a globally prevalent cancer. To understand its disease processes and the mechanisms of signaling regulation are critical issues. MicroRNAs (miRNAs) are small non-coding RNAs, involved in the modulation of physical or pathological properties. miRNAs are also important regulators in OC pathogenesis. miR-125 family genes are involved in the disease process of a wide variety of cancers. In colorectal cancer and breast cancer, it acts as tumor suppressor. However, in non-small cell lung cancer and leukemia, miR-125 is oncogenic. Thus, there are controversies regarding the functions of miR-125 in different types of cancers. It appears that miR-125 is down-regulated in OC, but the carcinogenic mechanisms and the signaling impacts of miR-125 in OC are still obscure. In silico modules predict that FAM213A (Family with sequence similarity 213, member A) is a potential target of miR-125. FAM213A is a known anti-oxidant protein that protects cell from oxidative stress. Our previous study revealed that FAM213A was up-regulated in OC tumors. This study further specifies that miR-125 expression is down-regulated in OC tumors and cell lines. Besides, lower miR-125b expression in OC tissues is associated with the worse prognosis in stage I and II patients. We also identified that miR-125b targeted the 3’UTR of FAM213A to repress its gene activity. This targeting is accompanied with the increase of oxidative stress. Exogenous miR-125b expression decreased the oncogenicity of OC cell. miR-125b and FAM213A drive opposite oncogenic phenotypes. OC cell clones stably express complete FAM213A transcript have been established in our work. We are about to carry out rescue experiments and tumorigenic studies using these clones to further specify the roles of miR-125b-FAM213A regulatory axis in OC induction.
|
|---|
