Xiangrui Meng^*1, Xiaoqi Chen^†1, Peng Lu^‡, Wang Ma^*, Dongli Yue^*, Lijie Song^*, Qingxia Fan^*

Oncology Research, Vol.25, No.2, pp. 215-223, 2017, DOI:10.3727/096504016X14732772150541

Abstract Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant cancers with high mortality around the world. However, the regulatory mechanism of ESCC carcinogenesis is not completely known. Here we demonstrate the novel role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained from the GEO database showed that the expression of miR-202 is aberrantly decreased in tumor tissue from ESCC patients and cultured ESCC cell lines. After transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC cells was significantly increased by miR-202 overexpression but reduced by miR-202… More >

Dayong Yan^*1, Xiaoqing Cai^*1, Yu Feng^†

Oncology Research, Vol.24, No.6, pp. 399-404, 2016, DOI:10.3727/096504016X14685034103239

Abstract This study was designed to investigate the role of miR-183 in modulating cell growth and apoptosis of tongue squamous cell carcinoma SCC25 cell line. Human squamous epithelial cell and squamous cell carcinoma cell line SCC25 was used, and miR-183 was inhibited. Cell growth, colony formation, and apoptotic rate, as well as the expression of caspase 3 and BCL-xL, were detected. Results showed that miR-183 was significantly overexpressed in the SCC25 cell line when compared with normal control. The miR-183 inhibitor reduced cell growth and colony formation, while the apoptosis percentage was significantly increased. The expression More >

Yangjing Chen, Ruimin Zhao, Qian Zhao, Yuan Shao, Shaoqiang Zhang

Oncology Research, Vol.24, No.3, pp. 153-160, 2016, DOI:10.3727/096504016X14612603423476

Abstract Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a corepressor for the transcription factor PBX. Previous studies showed that HPIP is frequently overexpressed in many tumors. However, the role of HPIP in head-and-neck squamous cell carcinoma (HNSCC) has not yet been determined. Thus, we decided to investigate the effects and mechanisms of HPIP in HNSCC. Our results demonstrated that HPIP is highly expressed in human HNSCC cell lines and provides the first evidence that knockdown of HPIP obviously inhibits proliferation and migration/invasion in HNSCC cells in vitro, as well as inhibits tumor growth in More >

Arya Sobhakumari^*1, Kevin P. Orcutt^†‡1, Laurie Love-Homan^§, Christopher E. Kowalski^†‡, Arlene D. Parsons^†, C. Michael Knudson^†‡§¶, Andrean L. Simons^*†‡§¶

Oncology Research, Vol.24, No.1, pp. 55-64, 2016, DOI:10.3727/096504016X14586627440192

Abstract Poor tumor response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is a significant challenge for effective treatment of head and neck squamous cell carcinoma (HNSCC). Therefore, strategies that may increase tumor response to EGFR TKIs are warranted in order to improve HNSCC patient treatment and overall survival. HNSCC tumors are highly glycolytic, and increased EGFR signaling has been found to promote glucose metabolism through various mechanisms. We have previously shown that inhibition of glycolysis with 2-deoxy-d-glucose (2DG) significantly enhanced the antitumor effects of cisplatin and radiation, which are commonly used to treat… More >

MI HEON RYU^1,a, JEONG HEE PARK^1,a, JI EUN PARK¹, JIN CHUNG², CHANG HUN LEE³AND HAE RYOUN PARK^1*

BIOCELL, Vol.34, No.1, pp. 15-22, 2010, DOI:10.32604/biocell.2010.34.015

Abstract Tumor cells are often found under hypoxic conditions due to the rapid outgrowth of their vascular supply, and, in order to survive hypoxia, these cells induce numerous signaling factors. Akt is an important kinase in cell survival, and its activity is regulated by the upstream phosphoinositide 3-kinase (PI3K) and receptor tyrosine kinases (RTKs). In this study, we examined Akt activation and RTKs/PI3K/Akt signaling using the hypoxia-mimetic cobalt chloride in oral squamous carcinoma cells. Cobalt chloride increases Akt phosphorylation in both a dose- and time-dependent manner. Blocking the activation of the PI3K/Akt pathway using LY294002 abolished More >