Huang Li, Li Fang, Deng Pengbo, Hu Chengping

Oncology Research, Vol.24, No.6, pp. 405-413, 2016, DOI:10.3727/096504016X14685034103437

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More 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 >

Jing Li, Weixing Qu, Yazhou Jiang, Yi Sun, Yongyi Cheng, Tiejun Zou, Shuangkuan Du

Oncology Research, Vol.24, No.6, pp. 391-398, 2016, DOI:10.3727/096504016X14666990347518

Abstract MicroRNAs (miRNAs) have been shown to be involved in bladder cancer progression. miR-489 (also known as miR-489-3p) was recently reported to be a tumor suppressor in several cancers. However, its exact role and mechanism in the progression of bladder cancer are largely unknown. In this study, we explore the role of miR-489 in the proliferation and invasion of human bladder cancer cells. The miR-489 expression levels were detected in bladder cancer and normal adjacent tissues, as well as in human normal bladder epithelial cells and bladder cancer cell lines. The results showed that miR-489… More >

Feng Jiang^*1, Yan Shi^†1, Hong Lu^†, Guojun Li^*

Oncology Research, Vol.24, No.5, pp. 381-389, 2016, DOI:10.3727/096504016X14685034103392

Abstract Armadillo repeat-containing protein 8 (ARMC8) plays an important role in regulating cell migration, proliferation, tissue maintenance, signal transduction, and tumorigenesis. However, the expression pattern and role of ARMC8 in osteosarcoma are still unclear. In this study, our aims were to examine the effects of ARMC8 on osteosarcoma and to explore its underlying mechanism. Our results demonstrated that ARMC8 was overexpressed in osteosarcoma cell lines. Knockdown of ARMC8 significantly inhibited osteosarcoma cell proliferation in vitro and markedly inhibited xenograft tumor growth in vivo. ARMC8 silencing also suppressed the epithelial– mesenchymal transition (EMT) phenotype, as well as More >

Tao Liang, Xiao-Yong Hu, Yong-Hui Li, Bin-Qiang Tian, Zuo-Wei Li, Qiang Fu

Oncology Research, Vol.24, No.5, pp. 371-380, 2016, DOI:10.3727/096504016X14685034103356

Abstract MicroRNA-21 (miRNA-21), a kind of short, noncoding RNAs, functioned as a tumor marker and was upregulated in renal cell carcinoma (RCC). However, the underlying mechanisms of miRNA-21 in RCC were uncertain. Therefore, the effects and mechanisms of miRNA-21 on the proliferation, differentiation, and apoptosis of cultured human RCC cells were further investigated in this study. After slicing miRNA-21 in RCC cells, the viability, mRNA expression of C/EBPα and PPARγ, caspase 3 activity, and protein expression of mTOR, STAT3, and pSTAT3 were determined. It was found that knockdown of miRNA-21 downregulated the optical density (OD) value More >

Yu Wang^*†1, Hui Leng^†1, Hui Chen^*‡, Lei Wang^*, Nan Jiang^*, Xin Huo^†, Bin Yu^*

Oncology Research, Vol.24, No.5, pp. 361-369, 2016, DOI:10.3727/096504016X14685034103310

Abstract Ubiquitin-conjugating enzyme E2T (UBE2T), a member of the E2 family, was found to be overexpressed in a great many cancers such as bladder cancer, lung cancer, and prostate cancer. However, there have been no reports on the role of UBE2T in osteosarcoma. In this study, we tried to make the effects of UBE2T on osteosarcoma clear. The study results showed that UBE2T was overexpressed in osteosarcoma tissues and cell lines. Moreover, UBE2T knockdown inhibited osteosarcoma cell proliferation, migration, and invasion. We also observed that UBE2T downregulation could suppress the activity of the PI3K/Akt signaling pathway. More >

Min Zhao^*, Zhiying Su^†, Shiyang Zhang^‡, Liangjin Zhuang^§, Yudi Xie^*, Xiaodong Li^*

Oncology Research, Vol.24, No.5, pp. 353-360, 2016, DOI:10.3727/096504016X14685034103275

Abstract Ovarian cancer (OC) is one of the most common gynecological malignancies. MicroRNAs (miRs) play a crucial role in the development and progression of OC, but the underlying mechanism remains largely unclear. Our study investigated the regulatory role of miR-148a in OC cell proliferation and invasion. We found that miR- 148a was significantly downregulated in OC tissues compared to their matched adjacent nontumor tissues. In addition, its expression was also reduced in OC cell lines (SKOV3, ES-2, OVCAR, and A2780) compared to normal ovarian epithelial cells. Overexpression of miR-148a caused a significant decrease in OC cell… More >

Wang Weihua, Chen Jie, Dai Jinhua, Zhang Burong, Wang Feng, Sun Yizhe

Oncology Research, Vol.24, No.5, pp. 345-351, 2016, DOI:10.3727/096504016X14685034103194

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More >

Xuexin Gao^*, Xuezhen Gao^†, Chao Li^*, Yukun Zhang^*, Lei Gao^‡

Oncology Research, Vol.24, No.5, pp. 337-343, 2016, DOI:10.3727/096504016X14666990347671

Abstract Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G₀/G₁ phase in More >

Makoto Isono, Akinori Sato, Kazuki Okubo, Takako Asano, Tomohiko Asano

Oncology Research, Vol.24, No.5, pp. 327-335, 2016, DOI:10.3727/096504016X14666990347635

Abstract The histone deacetylase (HDAC) inhibitor belinostat increases the amount of unfolded proteins in cells by promoting the acetylation of heat shock protein 90 (HSP90), thereby disrupting its chaperone function. The human immunodeficiency virus protease inhibitor ritonavir, on the other hand, not only increases unfolded proteins by suppressing HSP90 but also acts as a proteasome inhibitor. We thought that belinostat and ritonavir together would induce endoplasmic reticulum (ER) stress and kill renal cancer cells effectively. The combination of belinostat and ritonavir induced drastic apoptosis and inhibited the growth of renal cancer cells synergistically. Mechanistically, the combination More >