Jian-Wei Wang, Xiao-Feng Wu, Xiao-Juan Gu, Xing-Hua Jiang

Oncology Research, Vol.27, No.9, pp. 979-986, 2019, DOI:10.3727/096504018X15336368805108

Abstract Cancer-associated fibroblasts (CAFs) play a predominant role in regulating tumor progression. Understanding how CAFs communicate with osteosarcoma is crucial for developing novel approaches for osteosarcoma therapy. Exosomes are able to transmit messages between cells. In this study, we demonstrated that CAFs transfer exosomes to osteosarcoma cells, which promotes osteosarcoma cell migration and invasion. Using a miRNA microarray analysis, we identified 13 miRNAs that are significantly increased in exosomes derived from cancer-associated fibroblasts (CAFs) and corresponding paracancer fibroblasts (PAFs). In vitro studies further validated that the levels of microRNA-1228 (miR-1228) were increased in CAFs, its secreted More >

Zhiqiang Liu^*1, Qiang Li^*1, Xin Zhao^†, Bin Cui^*, Libo Zhang^*, Qiang Wang^*

Oncology Research, Vol.26, No.9, pp. 1439-1446, 2018, DOI:10.3727/096504018X15189093975640

Abstract Numerous studies have suggested that microRNAs (miRNAs) are dysregulated in osteosarcoma (OS), implicating miRNAs in OS initiation and progression. Therefore, knowledge of aberrantly expressed miRNAs in OS may provide novel mechanistic insights into the tumorigenesis and tumor development of OS and facilitate therapeutic methods for patients with this aggressive bone neoplasm. In this study, data obtained from reverse transcription quantitative polymerase chain reaction (RT-qPCR) revealed that miR-935 was significantly decreased in OS tissues and cell lines. Restoration expression of miR-935 obviously restricted proliferation and invasion of OS cells. In addition, high-mobility group box 1 (HMGB1)… More >

Chengwei Zhou¹, Jianxiang Xu¹, Jinti Lin, Renjin Lin, Kai Chen, Jianzhong Kong, Xiaolong Shui

Oncology Research, Vol.26, No.9, pp. 1335-1343, 2018, DOI:10.3727/096504018X15188367859402

Abstract Long noncoding RNA (lncRNA) FEZF1-AS1 was demonstrated to facilitate cell proliferation and migration in some cancers. However, the functions of FEZF1-AS1 and its molecular mechanism in osteosarcoma remain to be elucidated. In our study, we found that the expression of FEZF1-AS1 was upregulated in osteosarcoma samples and cell lines compared with normal tissues or cells. Besides, we showed that the expression levels of FEZF1-AS1 in osteosarcoma patients were positively correlated with tumor metastasis and TNM stage. Additionally, FEZF1-AS1 knockdown inhibited cell proliferation, migration, and invasion in U2OS and MG63 cells, while upregulation had the opposite More >

Xuesong Wang^*, Yong Lin^†, Lei Peng^‡, Ruifu Sun^*, Xiaojin Gong^*, Jinlong Du^*, Xiugong Zhang^*

Oncology Research, Vol.26, No.6, pp. 933-940, 2018, DOI:10.3727/096504017X15144741233346

Abstract Osteosarcoma is one of the most aggressive malignancies with poor prognosis rates. Many studies have demonstrated that miRNAs were involved in osteosarcoma, but the role of miR-103a in osteosarcoma remains elusive. In this study, we detected the expression levels of miR-103 in osteosarcoma and non-osteosarcoma tissues and cell lines. The binding effect of miR-103 on p57 was detected by luciferase reporter assay. After altering expressions of miR-103 or p57, viability, migration, invasion, and apoptosis of MG63 cells and expressions of proteins related with the JNK/STAT and mTOR pathways were all detected. We found the higher More >

Gong-Yi Lv, Jun Miao, Xiao-Lin Zhang

Oncology Research, Vol.26, No.6, pp. 837-846, 2018, DOI:10.3727/096504017X14920318811721

Abstract Abnormal expression of long noncoding RNAs (lncRNAs) often contributes to the unrestricted growth and invasion of cancer cells. lncRNA X-inactive specific transcript (XIST) expression is upregulated in several cancers; however, its underlying mechanism in osteosarcoma (OS) has not been elucidated. In the present study, we found that XIST expression was significantly increased in OS tissues and cell lines by LncRNA Profiler and qRT-PCR. The effects of XIST and miR-320b on OS cell proliferation and invasion were studied by MTT and Transwell invasion assays. The competing relationship between XIST and miR-320b was confirmed by luciferase reporter More >

Chao Ma, Jinfeng Han, Dong Dong, Nanya Wang

Oncology Research, Vol.26, No.5, pp. 765-773, 2018, DOI:10.3727/096504017X15021536183535

Abstract MicroRNA-152 (miR-152) expression has been reported to be downregulated in osteosarcoma (OS). However, the role of miR-152 in OS is not well documented. In the present study, we aimed to explore the function and underlying mechanism of miR-152 in OS. We found that miR-152 was underexpressed in OS tissues and cell lines. Decreased miR-152 was inversely correlated with lymph node metastasis and advanced clinical stage. Overexpression of miR-152 significantly inhibited cell proliferation, colony formation, migration, and invasion of OS cells. Bioinformatics analyses showed that miR-152 directly targeted E2F transcription factor 3 (E2F3), as further confirmed More >

Daofu Jia^*, Yanping Niu^†, Dongling Li^‡, Zhaorui Liu^§

Oncology Research, Vol.26, No.5, pp. 753-764, 2018, DOI:10.3727/096504017X15024946480113

Abstract Osteosarcoma is a highly aggressive malignant bone tumor with poor prognosis. Evidence has suggested that lncRNAs are deregulated in multiple cancers. In this study, we investigated the role of the lncRNA C2dat1 on the biological functions of osteosarcoma cells. The expressions of C2dat1, miR-34a-5p, and Sirt1 in human osteosarcoma cells were altered by transfection with their specific vectors/shRNA or mimic/inhibitor. Cell viability, migration, invasion, and apoptosis were assessed posttransfection. The mRNA and protein levels of C2dat1, miR-34a-5p, and Sirt1 were detected by qRT-PCR and Western blot. The results showed that C2dat1 suppression reduced cell viability, More >

Heping Wang^*, Yanzhang Yu^†, Shuxin Fan^*, Leifeng Luo^*

Oncology Research, Vol.26, No.5, pp. 665-673, 2018, DOI:10.3727/096504017X14908298412505

Abstract Long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) has been confirmed to be involved in the progression of various cancers; however, its mechanism of action in osteosarcoma has not been well addressed. In our study, TUG1 was overexpressed and miR-153 was downregulated in osteosarcoma tissues and cell lines. A loss-of-function assay showed that TUG1 knockdown suppressed the viability, colony formation, and invasion of osteosarcoma cells in vitro. Moreover, TUG1 was confirmed to be an miR-153 sponge. Ectopic expression of TUG1 reversed the inhibitory effect of miR-153 on the proliferation and invasion of osteosarcoma cells. Further More >

Farui Sun^*, Yuanjin Zhang^*, Lijun Xu^*, Songbai Li^*, Xiang Chen^*, Ling Zhang^*, Yifan Wu^†, Jun Li^*

Oncology Research, Vol.26, No.4, pp. 655-664, 2018, DOI:10.3727/096504017X15119525209765

Abstract Although cisplatin has been shown to be an integral part of chemotherapy regimen in osteosarcoma (OS) treatment, toxicity issues and chemoresistance have hindered therapeutic development for OS. Exploring novel combination therapy methods is needed to circumvent the limitations of cisplatin alone. The proteasome inhibitor MG132 has shown antitumor effects in many solid tumors. However, little is known about its effects in combination with cisplatin in OS cells. In this study, we examined the effects of MG132 in combination with cisplatin in human OS cells (MG-63 and HOS). MG132 and cisplatin were applied to OS cells,… More >

Xiaoyan Wang^*, Yongguang Xu^*, Xinlei Chen^*, Jianmin Xiao^†

Oncology Research, Vol.26, No.3, pp. 495-502, 2018, DOI:10.3727/096504017X14982578608217

Abstract This study aimed to investigate the effect of dexmedetomidine (DEX) on osteosarcoma (OS) cell line MG63 and to explore the possible relationship between DEX and miR-520-3p in OS. The results showed that DEX could upregulate miR-520-3p, which directly targeted AKT1. Additionally, miR-520-3p also inhibited MG63 cell proliferation and migration, promoted apoptosis, and suppressed protein expressions of AKT, p-AKT, p-mTOR, and p-ERK1/2. DEX can inhibit OS cell proliferation and migration and promote apoptosis by upregulating the expression level of miR-520a-3p. DEX may serve as a potential therapeutic agent in OS treatment, and miR-520a-3p may be a More >