LICHEN XU^1,2, PAN ZHANG^3,*, GUIQI ZHANG², ZHAOLIANG SHEN⁴, XIZHUANG BAI^1,3,*

Oncology Research, Vol.32, No.11, pp. 1777-1789, 2024, DOI:10.32604/or.2024.047704 - 16 October 2024

Abstract Background: Osteosarcoma (OS), recognized as the predominant malignant tumor originating from bones, necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies. The role of fat mass and obesity-associated (FTO) in OS, particularly its correlation with malignant traits, and the fundamental mechanism, remains to be elucidated. Materials and Methods: 1. The FTO expression and survival rate in tumors were analyzed. 2. FTO in OS cell lines was quantified utilizing western blot and PCR. 3. FTO was upregulated and downregulated separately in MG63. 4. The impact of FTO on the… More >

Wenwei Jiang^*, Xinyu Cai^*, Tianyang Xu^*, Kaiyuan Liu^*, Dong Yang^*, Lin Fan^*, Guodong Li^*, Xiao Yu^†

Oncology Research, Vol.28, No.4, pp. 409-421, 2020, DOI:10.3727/096504020X15868639303417

Abstract Osteosarcoma (OS), the most common bone cancer, causes high morbidity in children and young adults. TRIM46 is a member of the family of tripartite motif (TRIM)-containing proteins that serve as important regulators of tumorigenesis. Here we investigate the possible role of TRIM46 in OS and the underlying molecular mechanism. We report an increase in the expression of TRIM46 in OS and its association with tumor size, Enneking’s stage, and patient prognosis. TRIM46 knockdown inhibits OS cell viability and cell cycle progression and induces apoptosis, while TRIM46 overexpression exerts inverse effects, which are inhibited by peroxisome… More >

Kejun Wang^*1, Lin Yan^*1, Fen Lu^†

Oncology Research, Vol.27, No.2, pp. 157-163, 2019, DOI:10.3727/096504018X15190861873459

Abstract miR-363-3p has been shown to suppress tumor growth and metastasis in various human cancers. However, the function of miR-363-3p in osteosarcoma (OS) has not been determined. In our study, we found that the expression of miR-363-3p was significantly downregulated in OS tissues compared with adjacent normal tissues. miR-363-3p expression was associated with the poor overall survival rate of OS patients. Moreover, we found that overexpression of miR-363-3p markedly inhibited the proliferation, migration, and invasion of U2OS and MG63 cells. Moreover, we found that SOX4 was a direct target of miR-363-3p in OS cells. Overexpression of 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 >

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 >

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 >

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 >