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Recently, microRNAs (miRNAs) have emerged as key factors involved in a series of biological processes, ranging from embryogenesis to programmed cell death. Its link to aberrant expression profiles has rendered it a potentially attractive tool for the diagnosis, prognosis, or treatment of various diseases. Accumulating evidence has indicated that miRNAs act as tumor suppressors in hepatocyte malignant transformation by regulating development, differentiation, proliferation, and tumorigenesis. Here, we summarize recent progress in the development of novel biomarker-based miRNA therapeutic strategies for hepatocellular carcinoma (HCC).

Background and Objective Octamer-4 (Oct4), a transcription factor involved in regulating human embryonic stem cells (ESCs), may play a role in tumorigenesis. Since little is known about the efficacy of Oct4 as a potential biomarker for gastric cancer (GC), we investigated its expression in GC tissues and its relationship to various clinicopathological parameters. Methods Primary tumor tissues and matching, adjacent non-cancerous tissues were obtained from 62 GC patients, and Oct4 expression was examined by reverse transcription-PCR (RT-PCR) and real-time PCR. Twenty biopsy specimens of atrophic gastritis and gastric ulcer individually were collected as control. To detect Oct4 expression in the paired GC and non-cancerous tissues at the protein level, Western blotting and immunohistochemistry (IHC) were employed. Correlation analyses were conducted to assess the relationship between Oct4 expression and clinicopathological parameters. Results Oct4 expression levels were higher in GC tissues compared to matching, adjacent non-cancerous tissues, atrophic gastritis and gastric ulcer tissues. Additionally, Oct4 expression in GC tumors correlated with their differentiation status, but not with patient age or gender, tumor size, TNM stage, depth of invasion, or the presence of lymph node metastasis. Conclusions Oct4 may be a potential biomarker for the initiation, progression, and differentiation of human GC. J. Surg. Oncol. 2009;99:414–419. © 2009 Wiley-Liss, Inc.