Potential therapeutic implications of miRNAs in osteosarcoma chemotherapy

Chen, Dan; Ding, Lei; Chen, Zhiwei

doi:10.1177/1010428317705762

Cited by 14 publications

(13 citation statements)

References 70 publications

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“…Osteosarcoma is a type of malignant tumor characterized by strong local invasiveness (14, 15). According to a study, osteosarcoma patients with metastasis have strong resistance to chemotherapeutics, and approximately 30% of patients have no sensitivity to chemotherapeutics, which leads to poor clinical prognosis (16).…”

Section: Discussionmentioning

confidence: 99%

Expression of MiR-664-3p in Osteosarcoma and Its Effects on the Proliferation and Apoptosis of Osteosarcoma Cells

Li¹,

Tang²,

Hu³

et al. 2020

ijph

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Background: To explore the expression level of miR-664-3p in osteosarcoma and its effects on the proliferation and apoptosis of osteosarcoma cells. Methods: Specimens of osteosarcoma tissues were collected from 41 cases undergoing surgical treatment in the Orthopedics Department of Wuhan Puai Hospital, Wuhan, China from January 2015 to February 2018. Another 40 cases of normal bone tissue were collected. The expression of miR-664-3p were detected using quantificational real-time polymerase chain reaction. miR-664-3p mimics, miR-664-3p inhibitor and miR-664- 3p negative control (NC) were used to transfect U2-OS, which were named as mimics group, inhibitor group and NC group, respectively. MTT assay was adopted to detect the effects of microRNA-664-3p on the proliferation of U2-OS after 24, 48, 72, 96 and 120 hours of transfection. Flow cytometry was applied to measure the apoptosis rate of U2-OS after miR-664-3p transfection. Finally, Western Blot was employed to detect the expression of proteolipid protein 2 (PLP2). Results: The total apoptosis rate of cells in the inhibitor group was obviously higher than those in the mimics group and the NC group (P<0.001). The relative expression level of PLP2 in the inhibitor group was significantly lower than those in the mimics group and the NC group (P<0.001). Conclusion: MiR-664-3p may be involved in the occurrence and development of osteosarcoma, and can regulate the proliferation and apoptosis of U2-OS cells, and the expression of PLP2. Besides, miR-664-3p may become a novel molecular biological indicator for the diagnosis, targeted treatment and prognosis assessment of osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

Expression of MiR-664-3p in Osteosarcoma and Its Effects on the Proliferation and Apoptosis of Osteosarcoma Cells

Li¹,

Tang²,

Hu³

et al. 2020

ijph

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“…The miRNAs and drug resistance relationships in osteosarcoma have been identified, which further broadens the knowledge of the structure and functions of miRNAs in the disease (33). It has been predicted that miRNAs will reverse chemotherapy resistance in future analyses (34). miR-216b is a member of the miR-216 cluster and is located on human chromosome 2p16.1 (35).…”

Section: Discussionmentioning

confidence: 99%

Thiostrepton and miR‑216b synergistically promote osteosarcoma cell cytotoxicity and apoptosis by targeting FoxM1

Cai

Xiao²,

Shen³

et al. 2020

Oncol Lett

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Osteosarcoma is a common primary bone cancer that there are currently no effective treatment strategies for. Forkhead box M1 (FoxM1) is key in the development of osteosarcoma, and microRNA (miR)-216b serves an antitumor role by targeting FoxM1. Moreover, thiostrepton (TST), a natural thiazole antibiotic, induces antitumor effects and specifically targets FoxM1. Therefore, the present study investigated whether thiostrepton and miR-216b synergistically inhibited osteosarcoma cells by targeting FoxM1. The MTT assay, reverse transcription-quantitative PCR, a dual-luciferase reporter assay and flow cytometry were performed. Compared with the human osteoblast cell line hFOB1.19, miR-216b expression was significantly downregulated in the osteosarcoma cell lines U2OS, MG63 and Saos-2. By contrast, FoxM1 expression was significantly upregulated in osteosarcoma cell lines compared with the hFOB1.19 cell line. The results indicated that miR-216b targeted the 3'-untranslated region of FoxM1. Moreover, the results suggested that miR-216b cooperated with TST to decrease cell cytotoxicity and increase cell apoptosis. In addition, miR-216b cooperated with TST to increase Bax expression and decrease Bcl-2 expression. In conclusion, the combination of TST and miR-216b synergistically promoted osteosarcoma cell cytotoxicity and apoptosis by targeting FoxM1. Therefore, the present study suggested that the combination of TST and miR-216b may serve as a promising therapeutic strategy for osteosarcoma.

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“…Zhang, et al17 found that miR-4443 depletion increases the sensitivity of epirubicin-resistant H1299 cells to epirubicin by decreasing the IC50 of epirubicin and inducing cell apoptosis and G0/G1 cell cycle arrest in non-small cell lung cancer. Additionally, previous studies have demonstrated that miRNAs are also correlated with chemosensitivity in osteosarcoma 18. For example, miR-125b was found to enhance chemosensitivity to cisplatin in osteosarcoma 19.…”

Section: Introductionmentioning

confidence: 89%

miR-1301/TRIAP1 Axis Participates in Epirubicin-Mediated Anti-Proliferation and Pro-Apoptosis in Osteosarcoma

et al. 2019

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Purpose Epirubicin is one of the most effective drugs against osteosarcoma. miR-1301 is involved in the occurrence and development of osteosarcoma. Whether miR-1301 is responsible for the chemosensitivity of osteosarcoma cells to epirubicin remains largely unknown. Materials and Methods U2OS and SAOS-2 cells were treated with various concentrations of epirubicin. Flow cytometry was employed to evaluate cell apoptotic rate. Cell proliferation was measured by Cell Counting Kit-8 assay. Western blot and quantitative real-time polymerase chain reaction were utilized to detect the expressions of B-cell lymphoma-2 (Bcl-2), Bcl-2 assaciated X protein (Bax), cleaved-caspase-3, cleaved-poly (ADP-ribose) polymerases (PARP1), TP53-regulated inhibitor of apoptosis 1 (TRIAP1), and microRNA-1301 (miR-1301). The relationship between miR-1301 and TRIAP1 was determined by luciferase reporter assay. Results Epirubicin inhibited proliferation in a dose-dependent manner, induced apoptosis, decreased the expression of Bcl-2, and increased the expressions of Bax, cleaved-caspase-3, and cleaved-PARP1 in osteosarcoma cells. miR-1301 was downregulated in U2OS and SAOS-2 cells. Importantly, epirubicin significantly increased the levels of miR-1301. Overexpression of miR-1301 suppressed proliferation and promoted apoptosis. Interestingly, those effects were enhanced by epirubicin. In contrast, miR-1301 depletion attenuated the epirubicin-mediated anti-osteosarcoma effect. miR-1301 negatively regulated the expression of TRIAP1 in U2OS and SAOS-2 cells. Furthermore, epirubicin inhibited the mRNA and protein levels of TRIAP1 by upregulating miR-1301 levels. Epirubicin suppressed cell proliferation by downregulating TRIAP1. Conclusion miR-1301 was implicated in the chemosensitivity of osteosarcoma to epirubicin by modulating TRIAP1.

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Potential therapeutic implications of miRNAs in osteosarcoma chemotherapy

Cited by 14 publications

References 70 publications

Expression of MiR-664-3p in Osteosarcoma and Its Effects on the Proliferation and Apoptosis of Osteosarcoma Cells

Expression of MiR-664-3p in Osteosarcoma and Its Effects on the Proliferation and Apoptosis of Osteosarcoma Cells

Thiostrepton and miR‑216b synergistically promote osteosarcoma cell cytotoxicity and apoptosis by targeting FoxM1

miR-1301/TRIAP1 Axis Participates in Epirubicin-Mediated Anti-Proliferation and Pro-Apoptosis in Osteosarcoma

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