TGF-β1-induced miR-202 mediates drug resistance by inhibiting apoptosis in human osteosarcoma

Zx, Lin; Song, Dianwen; Wei, Haifeng; Yang, Xinghai; Liu, Tielong; Yan, Wangjun; Xiao, Jianru

doi:10.1007/s00432-015-2028-9

Cited by 36 publications

(28 citation statements)

References 21 publications

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“…Other studies indicate a physiological association between increases in follicular miRNA levels and hormone secretion levels in mammals, which involved signaling pathways involved in follicular cell proliferation, steroidogenesis, prevention of premature luteinization, and oocyte maturation (Sontakke et al, 2014;Donadeu et al, 2016;Xie et al, 2016). miR-202 inhibits tumor progression and (Farhana et al, 2015;Lin et al, 2016;Meng et al, 2016) affects the immune system (Fornari et al, 2015;Owen et al, 2015). miRNAs regulate levels of expression of target genes by controlling the signal pathways (Š ahmatova et al, 2016;Wang et al, 2016).…”

Section: Discussionmentioning

confidence: 94%

Differential Expression of miR-202 and Validation of Predicted Target Genes in the Skin Tissue of C57BL/6 Black Mice and BALB/c White Mice

Liu

Zhao

et al. 2017

DNA and Cell Biology

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In recent years, with the need of the fur industry to obtain greater quantities of high-quality fur and the research of hair follicle development attracting greater attention, the role of miRNAs in hair follicle development has become a field of intense interest. miRNAs are short length RNAs that affect gene regulation by binding to the 3'-untranslated region (3'UTR) of the mRNAs of certain target genes. This study predicted and validated the target genes of miR-202 in the skin tissue of C57BL/6 black mice and BALB/c white mice. The expression of miR-202 target genes (wnt5a, kit, and tcf7) was examined by real-time quantitative polymerase chain reaction and western blot in the mouse skin tissue and human embryonic kidney 293T cells (HEK293T cells) which overexpress miR-202. The luciferase reporter gene system was used to verify the correlation between the expression of miR-202 and its putative target genes. We show that the expression of miR-202 was higher in the skin tissue of C57BL/6 black mice than in the skin tissue of BALB/c white mice (p < 0.05). Furthermore, the expression of wnt5a, kit, and tcf7 was observed to be negatively correlated with the expression of miR-202 and to be downregulated by miR-202 in vitro and in vivo. The luciferase reporter gene system indicated that the target sequences of miR-202 are present in 3'UTR of wnt5a, kit, and tcf7 mRNAs. Altogether, this study has shown that the expression of miR-202 was different in the skin tissue of C57BL/6 black mice and BALB/c white mice and that wnt5a, kit, and tcf7 are negatively regulated by miR-202.

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Section: Discussionmentioning

confidence: 94%

Differential Expression of miR-202 and Validation of Predicted Target Genes in the Skin Tissue of C57BL/6 Black Mice and BALB/c White Mice

Liu

Zhao

et al. 2017

DNA and Cell Biology

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“…Increasingly, studies have shown that various miRNAs involved in apoptosis are also associated with chemotherapy resistance in osteosarcoma (22)(23)(24)(25). Some miRNAs function as oncogenes, and have been reported to be upregulated in osteosarcoma, while others serve as tumor suppressors, and are often downregulated in osteosarcoma (26).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-433 regulates apoptosis by targeting PDCD4 in human osteosarcoma cells

Sun

Wang

et al. 2017

Oncology Letters

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Abstract. Osteosarcoma is the most common aggressive sarcoma of the bone in children and adolescents. It is characterized by a high level of genetic instability and recurrent DNA deletions and amplifications. microRNAs (miRNAs) play a key role in cancer initiation, progression and metastasis; however, the potential role of miRNAs in osteosarcoma remains largely unknown. In the present study, miR-433 was shown to be overexpressed in osteosarcoma tissues compared with normal human osteoblasts. Transfection of miR-433 mimics into osteosarcoma cell lines significantly decreased apoptosis by targeting programmed cell death 4, a tumor suppressor that is involved in apoptosis. In contrast, inhibition of miR-433 enhanced apoptosis. Furthermore, in vivo miR-433 overexpression inhibited the apoptosis of tumor cells and increased tumor growth. The results of the present study suggested that miR-433 is a potential molecular target for osteosarcoma therapy.

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“…Besides, miR-15a, miR-16-1, miR-101, miR-34b, and miR-21 are shown to have the ability to increase chemosensitivity to anti-tumor drugs. 42,60,62,63 Table 1 and Figure 1 summarize the ongoing basic researches of miRNAs relating to chemosensitivity in osteosarcoma. …”

Section: Mirnas Promoting Chemosensitivitymentioning

confidence: 99%

Potential therapeutic implications of miRNAs in osteosarcoma chemotherapy

2017

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Osteosarcoma is the most common primary bone cancer in young adults and adolescents. Drug resistance is the main cause leading to therapeutical failure. The mechanisms of drug resistance of osteosarcoma have not been fully understood. Notably, recent researches associate microRNA with drug resistance in osteosarcoma cells, raising the awareness that targeting microRNAs may help in chemotherapy success. In this review, we summarize the mechanisms linking microRNAs to drug resistance and ongoing researches on microRNAs in drug response to osteosarcoma. In addition, the therapeutic potential of microRNAs in chemotherapy will also be discussed.

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TGF-β1-induced miR-202 mediates drug resistance by inhibiting apoptosis in human osteosarcoma

Cited by 36 publications

References 21 publications

Differential Expression of miR-202 and Validation of Predicted Target Genes in the Skin Tissue of C57BL/6 Black Mice and BALB/c White Mice

Differential Expression of miR-202 and Validation of Predicted Target Genes in the Skin Tissue of C57BL/6 Black Mice and BALB/c White Mice

MicroRNA-433 regulates apoptosis by targeting PDCD4 in human osteosarcoma cells

Potential therapeutic implications of miRNAs in osteosarcoma chemotherapy

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