Increased expression of OCT4 is associated with low differentiation and tumor recurrence in human hepatocellular carcinoma.

Octamer binding transcription factor 4 (OCT4), a key transcription factor required to maintain self-renewal and pluripotency of human and mouse embryonic stem cells, has been recently identified to be associated with tumorigenesis and malignant transformation of many types of cancers. This study was to determine the roles of OCT4 in HCC recurrence and their impact on the clinical outcome of HCC patients. Western blot and immunohistochemical stains were used to detect the expression of OCT4 protein in 152 HCC tissues and 40 cirrhosis tissues, as well as in 6 human HCC cell lines and normal hepatocytes.

Down-regulation of RhoE is associated with progression and poor prognosis in hepatocellular carcinoma.

Background: RhoE is an atypical member of Rho GTPases family, which is a crucial regulator of cytoskeletal dynamics, cell cycle progression, and cell proliferation. Previous studies have reported that RhoE was aberrantly expressed in several human cancers, but the role of RhoE in hepatocellular carcinoma (HCC) remained poor understood.

Objectives: This study investigated the expression of RhoE and its clinical significance on the outcome of patients with HCC.

Up-regulated miR-17 promotes cell proliferation, tumour growth and cell cycle progression by targeting the RND3 tumour suppressor gene in colorectal carcinoma.

Emerging evidence indicates that the miR-17 family may have a causal role in human cancer tumorigenesis, but their specific effects on the occurrence of CRC (colorectal carcinoma) are still poorly understood. In the present study, we profiled CRC tissue samples by miRNA (microRNA) microarray and found that four members of the miR-17 family had higher expression in CRC tissues than in normal tissues. This finding was further validated by qRT-PCR (quantitative reverse transcription PCR).

Protein kinase CK2α is overexpressed in colorectal cancer and modulates cell proliferation and invasion via regulating EMT-related genes.

Background: Protein kinase CK2 is a highly conserved, ubiquitous protein serine/threonine kinase that phosphorylates many substrates and has a global role in numerous biological and pathological processes. Overexpression of the protein kinase CK2α subunit (CK2α) has been associated with the malignant transformation of several tissues, with not nearly as much focus on the role of CK2α in colorectal cancer (CRC). The aims of this study are to investigate the function and regulatory mechanism of CK2α in CRC development.

[Correlation of casein kinase 2β overexpression to the metastatic ability of colorectal cancer cells in vitro].

Objective: To investigate the expression of casein kinase 2β (ck2β) in colorectal cancer in relation to the metastatic ability of the cancer cells.

Methods: The expression of ck2β in 46 normal colorectal mucosa, 20 colorectal adenomas and 66 colorectal cancers were detected immunohistochemically. In colorectal cancer cells, Ck2β protein expression was knockdown by RNA interference using ck2β-specific small interfering RNA (siRNA) and the interference efficiency was assessed by Western blotting.

[Effect of protein kinase CK2 gene silencing on radiosensitization in human nasopharyngeal carcinoma cells].

Objective: To investigate the effect of protein kinase CK2 gene silencing on the radiosensitization in human nasopharyngeal carcinoma (NPC) cells and its possible mechanism.

Methods: RNA interference (RNAi) technique was used to down-regulate the protein kinase CK2alpha expression in 5-8F cells, and clonogenic assay was employed to observe the changes in the radiosensitivity of the cells. DNA double-strand break was assessed by immunofluorescence staining of gamma-H2AX foci, and the cell apoptosis was examined using Annexin V-FITC/PI double-staining flow cytometry.