Down-Regulation of miR-3928 Promoted Osteosarcoma Growth

Xu, Haidong; Liu, Xiaozhou; Zhao, Jianning

doi:10.1159/000358718

Cited by 32 publications

(23 citation statements)

References 31 publications

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“…Discussion miR-574 has been found to be upregulated in several types of cancers, including lung cancer, bladder cancer and prostate cancer (11)(12)(13)19). Foss et al (17) also suggested miR-574 as a serum biomarker of non-small cell lung cancer.…”

Section: Downregulation Of Mir-574-3p Inhibited Cell Growth and Inducmentioning

confidence: 94%

“…All diagnoses were based on pathological and/or cytological evidence (10). The histological features of the specimens were evaluated by senior pathologists according to the World Health Organization classification criteria (11)(12)(13). Tissues were obtained prior to chemotherapy and radiotherapy, and were immediately frozen and stored at -80˚C prior to reverse-transcription quantitative polymerase chain reaction (RT-qPCR) assay (3,5,10).…”

Section: Methodsmentioning

confidence: 99%

“…The critical functions of numerous miRNAs in cancer biology have been illustrated, including the regulation of various cellular processes, such as proliferation and apoptosis (3,5,9,10). The abnormality of miR-574-3p was observed in patients with non-small cell lung cancer and prostate cancer, and it was found that this miRNA regulated colorectal cancer growth and plays important roles in bladder cancer cell lines (11)(12)(13). Nevertheless, whether miR-574-3p participates in the progression of osteosarcoma remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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miR-574-3p acts as a tumor promoter in osteosarcoma by targeting SMAD4 signaling pathway

Liu

Zhou

et al. 2016

Oncology Letters

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Abstract. Human osteosarcoma is the most common primary bone malignancy sarcoma that affects primarily children and people <20 years old. In the present study, it was demonstrated that miR-574-3p was downregulated in human osteosarcoma U2OS, SAOS and MG63 cells lines as well as in osteosarcoma tissue compared with the normal tissues. Downregulation of miR-574-3p by antisense miR-574-3p, inhibited cell growth and induced cell apoptosis. Overexpression of miR-574-3p by transfection with miR-574-3p mimics promoted the growth of U2OS cells. The present study then identified mothers against decapentaplegic homolog 4 (SMAD4) as a target of miR-574-3p and SMAD4 was suppressed in miR-574-3p transfected cells. Overexpression of SMAD4 could rescue the promoting effects of miR-574-3p on cancer cell growth. In conclusion, miR-574-3p exerts tumor-promoting roles by targeting the tumor-suppressing gene SMAD4 and its downstream signaling in human osteosarcoma, which provides a novel target for the treatment.

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Section: Downregulation Of Mir-574-3p Inhibited Cell Growth and Inducmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-574-3p acts as a tumor promoter in osteosarcoma by targeting SMAD4 signaling pathway

Liu

Zhou

et al. 2016

Oncology Letters

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“…FACS analysis was performed as previously described [25]. Cell apoptosis was determined using an annexin V-FITC apoptosis detection kit (BD Biosciences).…”

Section: Methodsmentioning

confidence: 99%

Midazolam Inhibits the Apoptosis of Astrocytes Induced by Oxygen Glucose Deprivation via Targeting JAK2-STAT3 Signaling Pathway

Liu

You²,

Tu³

et al. 2015

Cell Physiol Biochem

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Background: There is an increasing interest in the role of astrocytes contributing to the intrinsic bioremediation of ischemic brain injury. The purpose of this study was to disclose the effects and mechanism of midazolam (MDZ) on the proliferation and apoptosis of astrocytes under oxygen glucose deprivation (OGD) condition. Methods: The astrocytes were assigned randomly into four groups: control group, OGD group, OGD+MDZ group, and OGD+MDZ+IL-6 group. The astrocytes were treated with MDZ at dose of 10 μmol/L in OGD+MDZ group. And in OGD+MDZ+IL-6 group, the astrocytes were treated with MDZ at dose of 10μmol/L and IL-6 at dose of 50 ng/mL. MTT assay was used to assess cell proliferation, and cell apoptosis was analyzed by TUNEL apoptosis assay kit and flow cytometry. Furthermore, the expression of JAK2, p-JAK2, STAT3, p-STAT3, Bcl-2, Bax and Caspase-3 proteins were determined by western blotting assay. Results: Astrocytes proliferation was decreased obviously in OGD group, while MDZ could increase astrocytes proliferation under OGD condition. Moreover, OGD could induce apoptosis in astrocytes and MDZ could play an anti-apoptotic role. However, IL-6, a JAK2 activator, could attenuate cell proliferation and anti-apoptotic effects of MDZ in astrocytes. In addition, the expression of Bcl-2 protein in MDZ group increased markedly, while the JAK2/STAT3 signal proteins, Bax and Caspase-3 proteins decreased relative to OGD group. But IL-6 could counteract the anti-apoptotic effects of MDZ. Conclusion: Midazolam has protective effects on the proliferation and apoptosis of astrocytes via JAK2/STAT3 signal pathway in vitro. We firstly disclose the beneficial roles of midazolam in astrocytes under ischemic condition, which may be a rational treatment selection for ischemic cerebral protection.

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“…Ankur et al showed that up-regulation of miR-100 inhibited mTOR signaling and enhanced sensitivity to RAD001 [58]. Interestingly, Huang and his colleagues identified for the first time that miR-100 might act as a tumor suppressor in the progression of osteosarcoma by controlling the direct target gene Cyr61 [75,99]. It has been reported that Cyr61 promotes cell proliferation and inhibit cell apoptosis by binding to different types of integrin molecules, which resulted in down-regulating p53 expression and up-regulating NF-κB expression through PI3K/Akt/ mTOR pathways [100,101].…”

Section: Mir-100 In Cancer Proliferation and Apoptosismentioning

confidence: 99%

Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

Li¹,

Gao²,

Zhang³

et al. 2015

Cell Physiol Biochem

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MicroRNAs (miRNAs) are a recently discovered class of endogenous, small (about 22 nucleotides) non-coding RNAs, which play important roles in cancer development and progression. Emerging evidence shows that microRNAs exert their regulatory effects by directly binding to the 3'- untranslated regions (UTRs) of their target genes. MicroRNA-100 (miR-100) is aberrantly expressed and functions in many human cancers by regulating multiple cell processes, such as cell cycle, proliferation, differentiation, migration, invasion and apoptosis, via post-transcriptionally regulating various target genes. A better understanding of the molecular mechanisms involved in miR-100-mediated tumor progression will provide an opportunity for exploring novel miR-100-based targeted therapies for human cancers. This review aims to summarize the recently published literature on the roles of miR-100 in regulating tumorigenesis, and explore its potential clinical applications for cancer diagnosis, prognosis and clinical treatment.

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Down-Regulation of miR-3928 Promoted Osteosarcoma Growth

Cited by 32 publications

References 31 publications

miR-574-3p acts as a tumor promoter in osteosarcoma by targeting SMAD4 signaling pathway

miR-574-3p acts as a tumor promoter in osteosarcoma by targeting SMAD4 signaling pathway

Midazolam Inhibits the Apoptosis of Astrocytes Induced by Oxygen Glucose Deprivation via Targeting JAK2-STAT3 Signaling Pathway

Multiple Roles of MicroRNA-100 in Human Cancer and its Therapeutic Potential

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