miR-19 promotes osteosarcoma progression by targeting SOCS6

Sun, Zhengwen; Liu, Qingxia; Hong, Huanyu; Zhang, Haiguang; Zhang, Tongqing

doi:10.1016/j.bbrc.2017.10.002

Cited by 25 publications

(19 citation statements)

References 35 publications

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“…Recent research found that miR-19 could activate JAK2/STAT3 signaling pathway via silencing SOCS6 and in osteosarcoma and promote osteosarcoma growth in vitro and in vivo, including the reduction of G1-S arrest and an increase of the S phase 36 . JAK2/STAT3 signaling pathway is one of the critical signaling pathways involved in the development and homeostasis in mammals and recent has been reported to involves in the pathogenesis of various cancers including BC 37 , 38 .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA neuroblastoma-associated transcript 1 gene inhibits malignant cellular phenotypes of bladder cancer through miR-21/SOCS6 axis

2018

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Bladder cancer (BC) is one of the most common tumors in the urinary system. Noncoding RNAs are considered to take part in cellular phenotypes and are emerging as diagnostic and prognostic biomarkers of BC. The aim of this study is to investigate the clinical significance of neuroblastoma- associated transcript 1 (NBAT1) gene and its effects on malignant cellular phenotypes in BC. NBAT1 gene was low-expressed in BC tissues and cell lines and its low-expression was related with high pathological grade and metastasis of BC. Upregulation of NBAT1 gene depressed cell viability and invasiveness of KK47 and T24 cells and arrested KK47 and T24 cells at G1 stage. In addition, NBAT1 could target silence the expression of miR-21-5p in RNA-induced silencing complex-dependent manner. KK47 and T24 cells with miR-21-5p knockdown showed reduced cell viability, G1-stage arrest, and depressed invasiveness. MiR-21-5p mediates the regulatory effects of NBAT1 on malignant cellular phenotypes of BC cells. Moreover, SOCS6 gene was a target gene of miR-21-5p, and miR-21-5p modulated malignant cellular phenotypes of KK47 and T24 cells through targeted silencing of SOCS6. In conclusion, low-expression of NBAT1 is associated with the progress and metastasis of BC, and NBAT1 inhibits malignant cellular phenotypes through miR-21-5p/SOCS6 axis in BC. Our findings help to elucidate the tumorigenesis of BC, and future study will provide a novel therapeutic target for BC.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA neuroblastoma-associated transcript 1 gene inhibits malignant cellular phenotypes of bladder cancer through miR-21/SOCS6 axis

2018

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“…Osteosarcoma is one common bone tumor which affects more and more children globally. At present, the primary treatments for osteosarcoma are radiotherapy, chemotherapy and surgical resection ( 22 ). Although great efforts have been made to explore the underlying mechanisms of osteosarcoma carcinogenesis, the prognosis is still unsatisfied due to extremely-high metastatic rate as well as aggressive invasion into local tissues ( 23 , 24 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑210 promotes human osteosarcoma cell migration and invasion by targeting FGFRL1

et al. 2018

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Osteosarcoma is a common bone tumor and a frequently occuring cancer-associated threat to children. Notably, the prognosis of osteosarcoma is very poor when it is diagnosed with metastasis. A growing number of studies have indicated that various microRNAs (miRs) serve important regulatory roles in the pathogeny of different types of cancer. However, the functions of miR-210 in osteosarcoma need to be elucidated comprehensively. The aim of the present study was to investigate the potential roles of miR-210 in osteosarcoma by targeting fibroblast growth factor receptor-like 1 (FGFRL1). Reverse transcription-quantitative polymerase chain reaction results revealed that the expression of miR-210 was highly elevated while FGFRL1 expression was reduced inversely in osteosarcoma tissues compared with matched normal tissues. The results of Transwell assays showed that miR-210 promoted osteosarcoma cell migration and invasion. Furthermore, the luciferase reporter assay results suggested that miR-210 could directly bind to FGFRL1 in osteosarcoma cells. In addition, the present findings demonstrated that miR-210 could negatively regulate FGFRL1 expression by targeting the 3′untranslated region. In conclusion, the findings of the present study suggested that miR-210 exerted tumor carcinogenic functions in osteosarcoma by targeting FGFRL1. The findings of this study demonstrated that FGFRL1 was a direct target of miR-210 in osteosarcoma involved in the promoting functions mediated by miR-210 in the invasion and migration of osteosarcoma, suggesting that miR-210/FGFRL1 may be promising for discovering diagnostic and prognostic biomarkers for the therapies of osteosarcoma.

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“…We chose to study miR-19b because it was the only member of the miR-17-92 cluster to be downregulated in the infarct area following IR injury [27]. miR-19 has also been found to promote the progression of osteosarcoma by targeting and downregulating SOCS-6 in association with JAK2/STAT3 signaling [36]. The JAK2/STAT3 signaling pathway is involved in the progression of several cancers and is associated with other SOCS proteins through feedback regulation in various cell processes [37][38][39][40].…”

Section: Discussionmentioning

confidence: 99%

SOCS-6 promotes mitochondrial fission and cardiomyocyte apoptosis and is negatively regulated by QKI mediated miR-19b

Zhang¹,

Guan²,

Ye³

et al. 2020

Preprint

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Background Ischemia/reperfusion (IR) injury following myocardial infarction can result in debilitating complications and morbidity. Mitochondrial dysfunction and abnormal mitochondrial fission have been implicated in the complications associated with IR injury as cardiomyocytes are abundant in mitochondria. SOCS-6 is known to participate in mitochondrial fragmentation but its exact involvement and the pathways associated are uncertain. Results In the present study, we examine the biological role and regulation of SOCS-6 in mitochondrial dynamics using hypoxia and reoxygenation (H/R) in cardiomyocytes and with a murine model of IR injury. We found that SOCS-6 inhibition by RNA interference attenuated H/R-induced mitochondrial fission and apoptosis in cardiomyocytes. A luciferase assay indicated that SOCS-6 is a direct target of miR-19b. The overexpression of miR-19b decreased mitochondrial fission and apoptosis in vitro . Moreover, the presence of miR-19b reduced the level of SOCS-6 and the injury caused by IR in vivo . There were less apoptotic cells in the myocardium of mice injected with miR-19b. In addition, we found that the RNA-binding protein, QKI, participates in the regulation of miR-19b expression. Conclusions Our results indicate that the inhibition of mitochondrial fission through downregulating SOCS-6 via the QKI/miR-19b/SOCS-6 pathway attenuated the damage sustained by IR. The QKI/miR-19b/SOCS-6 axis plays a vital role in regulation of mitochondrial fission and cardiomyocyte apoptosis and could form the basis of future research in the development of therapies for the management of cardiac diseases.

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miR-19 promotes osteosarcoma progression by targeting SOCS6

Cited by 25 publications

References 35 publications

Long noncoding RNA neuroblastoma-associated transcript 1 gene inhibits malignant cellular phenotypes of bladder cancer through miR-21/SOCS6 axis

Long noncoding RNA neuroblastoma-associated transcript 1 gene inhibits malignant cellular phenotypes of bladder cancer through miR-21/SOCS6 axis

miR‑210 promotes human osteosarcoma cell migration and invasion by targeting FGFRL1

SOCS-6 promotes mitochondrial fission and cardiomyocyte apoptosis and is negatively regulated by QKI mediated miR-19b

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