Overexpression of TFIIB-related factor 2 is significantly correlated with tumor angiogenesis and poor survival in patients with esophageal squamous cell cancer.

Studies have shown that genetic activation of TFIIB-related factor 2 (BRF2) represents a unique mechanism of tumorigenesis through the increase in Pol III-mediated transcription. Several studies have shown that BRF2 is overexpressed in several types of cancer and suggest the oncogenic role of BRF2. This study aimed to examine the expression of TFIIB-related factor 2 (BRF2) in patients with esophageal squamous cell cancer (ESCC) and explore the relationship of BRF2 expression with clinicopathologic factors, tumor angiogenesis and prognosis. We found that increased BRF2 protein expression was prevalent in esophageal squamous cell cancer and was significantly associated with deeper tumor invasion (P = 0.039) and microvessel density (P = 0.007). Additionally, expression of BRF2 was found to be an independent prognostic factor in ESCC patients. Furthermore, a significant correlation between high BRF2 expression and shorter overall survival time was found in different subgroups of ESCC patients stratified by the clinical stage, T classification and lymph node metastasis. High expression of BRF2 protein is closely associated with tumor progression and angiogenesis and poor survival of ESCC. BRF2 is a promising biomarker to identify individuals with poor prognostic potential and concludes the possibility of its use as a prognostic marker in patients with ESCC.

General transcription factor IIb overexpression and a potential link to proliferation in human hepatocellular carcinoma.

The general transcription factor IIB (TFIIB) plays a central role in preinitiation complex (PIC) assembly, providing a bridge between promoter-bound TFIID and RNA Polymerase II (RNA POLII). TFIIB functionally counteracts the transcriptional activation of hepatitis B virus X protein (HBx), which has been shown to play a role in the development of human hepatocellular carcinoma (HCC). However, the function of TFIIB in HCC remains unclear. In this article, we demonstrate that TFIIB plays an important role in HCC pathogenesis. TFIIB expression was immunohistochemically examined in a series of 100 HCC tissue specimens. The expression level of TFIIB showed significant correlation with the histological grade (P = 0.030), the level of AFP (P = 0.011) and the proliferation marker Ki-67 (P = 0.0002). High TFIIB expression level correlated with poor survival. Western blot analysis also confirmed that the TFIIB protein was overexpressed in HCC tissue compared to benign normal tissue. Additionally, Western blot and qRT-PCR analyses showed a high expression level of TFIIB protein in the HCC cell lines SMMC7721, HepG2, BEL7404, and Huh7 and the immortalized normal line BEL7702 but a lower expression in the normal Chang hepatocyte cell line. Following the release of Huh7 cells from serum starvation, the expression of TFIIB was upregulated. A cell growth assay suggested that TFIIB was involved in the proliferation and growth of HCC cells. In conclusion, our results demonstrate that TFIIB overexpression may play essential roles in the pathogenesis of hepatocellular carcinoma by affecting the proliferation of HCC cells.

Transcription initiation factor IIB involves in Schwann cell differentiation after rat sciatic nerve crush.

Transcription Initiation Factor IIB (TFIIB), as a general transcription factor, plays an essential role in preinitiation complex assembly and transcription initiation by recruiting RNA polymerase II to the promoter. However, its distribution and function in peripheral system lesion and repair were still unknown. Here, we investigated the spatiotemporal expression of TFIIB in an acute sciatic nerve crush model in adult rats. Western blot analysis revealed that TFIIB was expressed in normal sciatic nerve. It gradually increased, reached a peak at the seventh day after crush, and then returned to the normal level at 4 weeks. We observed that TFIIB expressed mainly increased in Schwann cells and co-localized with Oct-6. In vitro, we induced Schwann cell differentiation with cyclic adenosine monophosphate (cAMP) and found that TFIIB expression was increased in the differentiated process. TFIIB-specific siRNA inhibited cAMP-induced Schwann cell morphological change and the expression of P0. Collectively, we hypothesized peripheral nerve crush-induced upregulation of TFIIB in the sciatic nerve was associated with Schwann cell differentiation.

Cloning, expression and functional characterization of Schizosaccharomyces pombe TFIIB.

The transcription factor TFIIB has been identified and cloned from the yeast Schizosaccharomyces pombe. The cloned polypeptide is highly homologous to human TFIIB and to Saccharomyces cerevisiae TFIIB. S. pombe TFIIB is a 340-amino-acid-long protein and it possesses a repeated motif of 75 amino acids near the carboxy-terminal region. The purified recombinant protein is able to bind to the TBP-DNA promoter complex in gel retardation experiments. Recombinant S. pombe TFIIB is active in in vitro transcription assays, since it can complement the transcription activity of a S. pombe cell extract in which TFIIB was depleted by using antibodies.