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 >

Wei Wang, Ke Zheng, Yi Pei, XiaoJing Zhang

Oncology Research, Vol.26, No.3, pp. 373-384, 2018, DOI:10.3727/096504017X14939809845080

Abstract JARID1B has been proven to be upregulated in many human malignancies and is correlated with tumor progression. However, its expression and clinical significance in osteosarcoma are still unclear. Thus, the aim of this study was to explore the effects of JARID1B in osteosarcoma tumorigenesis and development. In this study, we found that the expression levels of JARID1B in osteosarcoma tissues were significantly higher than those in corresponding noncancerous bone tissues. In addition, JARID1B upregulation occurred more frequently in osteosarcoma specimens from patients with a poor prognosis. After JARID1B transfection in osteosarcoma cells, cell proliferation was More >

Hai-Feng Zeng^*, Hai-Yan Qiu^†, Fa-Bo Feng^‡

Oncology Research, Vol.26, No.3, pp. 335-343, 2018, DOI:10.3727/096504017X14907375885605

Abstract Long noncoding RNAs (lncRNAs) have been verified to participate in various types of malignant tumors, including osteosarcoma (OS), which is the most common primary bone tumor with outstanding morbidity. Although an increasing number of lncRNAs have been reported to mediate the occurrence of OS, the potential mechanisms are still unclear. This study intends to uncover the mechanism by which lncRNA LINC01133 functions as an miRNA sponge to mediate OS tumorigenicity. In this study, we found that the expression level of LINC01133 was statistically upregulated in OS tumor tissue and cell lines compared to noncancerous tissues More >

Juntao Wang, Guodong Sun

Oncology Research, Vol.25, No.9, pp. 1517-1527, 2017, DOI:10.3727/096504017X14859934460780

Abstract miR-26a has been found to be downregulated in osteosarcoma (OS) when compared with normal control tissues and has been shown to suppress the malignant behaviors of OS cells. The underlying mechanism, nevertheless, remains unknown. In our study, the long noncoding RNA MALAT1, confirmed to be significantly upregulated in OS, is first shown to be capable of promoting proliferation and migration by directly suppressing miR-26a-5p in OS cells. In addition, we have identified forkhead box O1 (FOXO1) as a transcriptional factor of MALAT1 that can negatively regulate MALAT1. We have shown that MALAT1 promoted growth and More >

Shaokun Zhang^*, Lidi Liu^*, Zhenshan Lv^*, Qiao Li^*, Weiquan Gong^*, Hong Wu^†

Oncology Research, Vol.25, No.9, pp. 1505-1515, 2017, DOI:10.3727/096504017X14886485417426

Abstract Recent studies suggest that microRNAs (miRNAs) are critical regulators in many types of cancer, including osteosarcoma. miR-342-3p has emerged as an important cancer-related miRNA in several types of cancers. However, the functional significance of miR-342-3p in osteosarcoma is unknown. The aims of this study were to investigate whether miR-342-3p is dysregulated in osteosarcoma and to explore the biological function of miR-342-3p in regulating cellular processes of osteosarcoma cells. We found that miR-342-3p expression was significantly decreased in osteosarcoma tissues and cell lines. Overexpression of miR-342-3p inhibits the proliferation, migration, and invasion of osteosarcoma cells. In… More >

Boda Ying^*, Hong Huang^†, Hongfei Li^*, Meng Song^*, Sizhan Wu^*, Hongliang Ying^†

Oncology Research, Vol.25, No.9, pp. 1463-1470, 2017, DOI:10.3727/096504017X14878518291077

Abstract Procaine (PCA) is a conventional chemotherapeutic agent for osteosarcoma. Recent studies have proposed that the growth-inhibitory effect of PCA is through regulation of microRNAs (miRNAs). miR-133b has been proven to be a tumor suppressor in osteosarcoma, but whether it is involved in the antitumor effects of PCA on osteosarcoma has not been investigated. In this study, we aimed to explore the effects of PCA on osteosarcoma MG63 cells by regulation of miR-133b, as well as its underlying mechanisms. MG63 cells were treated with different concentrations of PCA, and cell viability, apoptosis, and miR-133b expression were… More >

Shi Ying^*, Huang Jianjun^†, Yi Xue^*, Yu Shuwei^*, Zhang Liyuan^*, Wang Jie^*, Cheng Lixian^*

Oncology Research, Vol.25, No.9, pp. 1421-1430, 2017, DOI:10.3727/096504016X14826089198805

Abstract MicroRNAs are a class of small noncoding RNAs that function as critical gene regulators through targeting mRNAs for translational repression or degradation. In this study, we showed that the miR-133b expression level was decreased while the Sirt1 mRNA expression level was increased in osteosarcoma tissue and cell lines. A low expression of miR-133b was significantly associated with tumor size, distant metastasis, and advanced clinical stage. In addition, osteosarcoma patients with a low miR-133b expression showed a worse prognosis when compared to those with a high level of miR-133b expression. Thus, we identified Sirt1 as a More >