Wenliang Liu^*, Peng Xiao^†, Han Wu^*, Li Wang^*, Demiao Kong^*, Fenglei Yu^*

Oncology Research, Vol.28, No.7-8, pp. 829-829, 2020, DOI:10.3727/096504021X16207253542097

Abstract This article has no abstract. More >

Wenliang Liu^*, Peng Xiao^†, Han Wu^*, Li Wang^*, Demiao Kong^*, Fenglei Yu^*

Oncology Research, Vol.25, No.6, pp. 975-988, 2017, DOI:10.3727/096504016X14791726591124

Abstract MicroRNAs (miRs) have been demonstrated to be significantly associated with the development and progression of non-small cell lung cancer (NSCLC). However, the underlying mechanism of miR-98 in mediating the malignant phenotypes of NSCLC cells remains obscure. In this study, we found that miR-98 was significantly downregulated in NSCLC tissues compared to nontumor lung tissues. Downregulation of miR-98 was significantly associated with poor differentiation and advanced clinical stage. Restoration of miR-98 expression significantly decreased the proliferation, migration, and invasion of NSCLC A549 and H1229 cells. SALL4 was identified as a target gene of miR-98, and the… More >

Yu Zhou, Yong Peng, Min Liu, Yugang Jiang

Oncology Research, Vol.25, No.6, pp. 947-957, 2017, DOI:10.3727/096504016X14791732531006

Abstract MicroRNAs (miRs), a class of noncoding RNAs that are 18–25 nucleotides in length, are able to suppress gene expression by targeting complementary regions of mRNAs and inhibiting protein translation. Recently, miR-181b was found to play a suppressive role in glioma, but the regulatory mechanism of miR-181b in the malignant phenotypes of glioma cells remains largely unclear. In this study, we found that miR-181b was significantly downregulated in glioma tissues when compared with normal brain tissues, and decreased miR-181b levels were significantly associated with high-grade pathology and a poor prognosis for patients with glioma. Moreover, miR-181b… More >

Dengfeng Zhang¹, Feng Jiang¹, Xiao Wang, Guojun Li

Oncology Research, Vol.25, No.5, pp. 763-771, 2017, DOI:10.3727/096504016X14772402056137

Abstract Sal-like protein 4 (SALL4) is a zinc finger transcription factor that has been reported to be aberrantly expressed in several human malignancies and identified as an oncogene. However, the potential role of SALL4 in osteosarcoma remains to be elucidated. In this study, we explored the biological functions of SALL4 in osteosarcoma. We found that SALL4 was overexpressed in osteosarcoma tissues and cell lines. Knockdown of SALL4 inhibited osteosarcoma cell proliferation, migration, and invasion in vitro. In addition, SALL4 knockdown suppressed osteosarcoma growth and metastasis in vivo. We also showed that SALL4 knockdown decreased the protein More >