MicroRNA-320a suppresses in GBM patients and modulates glioma cell functions by targeting IGF-1R

Guo, Tong; Feng, Ying; Liu, Qingyang; Yang, Xue; Jiang, Tao; Yan, Chen; Zhang, Quangeng

doi:10.1007/s13277-014-2283-4

Cited by 55 publications

(46 citation statements)

References 21 publications

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“…Overexpression of miR-133a directly suppresses the expression of IGF-1R at the mRNA level and protein level. In addition, it has been reported that abnormal expression of IGF-1R could affect multiple downstream signal pathways, PI3K/AKT and MAPK/ERK signaling pathways, which were involved in tumorigenesis and development [27,40]. Therefore, we investigated whether miR-133a affects activation of AKT and EKR pathways.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-133a functions as a tumor suppressor by targeting IGF-1R in hepatocellular carcinoma

Zhang

Liu

et al. 2015

Tumor Biol.

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MicroRNAs (miRNAs) are a class of small non-coding RNAs and have critical roles in tumorigenesis and metastasis. A growing body of evidence showed that microRNA-133a (miR-133a) was downregulated and played tumor suppressor roles in gastric, colorectal, bladder, and lung cancer. However, the role and underlying molecular mechanism of miR-133a in hepatocellular carcinoma (HCC) remain unclear. In this study, we analyzed the expression of miR-133a in HCC tissues and HCC cell lines. We find that miR-133a was downregulated in HCC tissues and cell lines and that miR-133a expression negatively correlated with tumor differentiation (P < 0.01), TNM stage (P < 0.01), and lymph node metastasis (P < 0.01). Then, functional studies demonstrate that restoration of miR-133a in HepG2 cells significantly suppressed proliferation, colony formation, migration, and invasion, induced cell cycle arrest at G0/G1 stage and cell apoptosis in vitro, and decreased tumor size and weight in a nude mouse HepG2 xenograft model. Using bioinformatics method and dual luciferase assays identified insulin-like growth factor 1 receptor (IGF-1R) as a direct target of miR-133a in HCC cells. Furthermore, overexpression of miR-133a inhibited activation AKT and ERK signal pathway, which contributed to suppression of HCC cell growth. These findings suggest that miR-133a may act as a tumor suppressor and inhibited survival of HCC cells by targeting IGF-1R.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-133a functions as a tumor suppressor by targeting IGF-1R in hepatocellular carcinoma

Zhang

Liu

et al. 2015

Tumor Biol.

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“…IGF1R likely performs its functions partly by participating in the regulation of AKT and ERK signalling pathways (26)(27)(28). To determine whether miR-495 is involved in the regulation of AKT and ERK pathways in HCC, we detected the expression levels of AKT, p-AKT, ERK and p-ERK in Hep3B cells transfected with miR-495 mimics or miR-NC.…”

Section: Mir-495 Attenuates Akt and Erk Signalling Pathways In Hccmentioning

confidence: 99%

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

Zhuang

Wang

et al. 2017

Exp Ther Med

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Abstract. Hepatocellular carcinoma (HCC) is the fifth most common malignancy and second-most frequent cause of cancer-associated deaths worldwide. Previously, increasing studies report that microRNAs (miRNAs/miRs) are abnormally expressed in various types of human cancers and may participate in the tumourigenesis and tumour development of HCC. miRNA-based targeted therapy is effective against different molecular targets and may increase the sensitisation of cancer cells to therapy by several folds. Therefore, further validation of potentially important miRNAs involved in HCC initiation and progression may provide valuable insights into the treatment of patients with HCC. miR-495 is abnormally expressed in multiple types of human cancers. However, the expression level and roles of miR-495 in HCC have yet to be completely elucidated. In the present study, miR-495 expression was frequently downregulated in HCC tissues and cell lines, and miR-495 expression levels were significantly correlated with tumour size, tumor-node-metastasis (TNM) stage and lymph node metastasis in patients with HCC. Functional assays revealed that miR-495 overexpression inhibited cell proliferation and invasion in HCC. Insulin-like growth factor receptor-1 (IGF1R) was identified as a direct target gene of miR-495 in HCC. IGF1R was upregulated in HCC tissues and negatively correlated with miR-495 expression level. The upregulation of IGF1R rescued the miR-495-induced tumour-suppressive roles in HCC cell proliferation and invasion, and the restored miR-495 expression inactivated the protein kinase B and extracellular regulated protein kinase signalling pathways in HCC. These results provide novel insights into the molecular mechanism underlying HCC progression, and suggest that miR-495 may be investigated as a novel therapeutic target for patients with this disease.

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“…In addition, overexpression of miR-320 resulted in the inhibition of cell proliferation, invasion, migration, and tumorigenesis by targeting IGF-1, which further regulated the signaling pathways downstream, such as phosphoInositide-3 kinase/ serine-threonine kinases (PI3K/AKT) and Mitogen-Activated Protein Kinase/ extracellular-response kinase (MAPK/ERK) [18]. Furthermore, a recent study has suggested that miR- 320 could inhibit tumor development and growth through targeting IGF-1, and miR-320 might act as a new effective target for the treatment of cancer [19]. MiR-320 inhibition also decreased ISW and ISW/AARW confirming that miR-320 inhibitors reduce infarct and thereby protect cardiac function.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of microRNA-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1

et al. 2016

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Insulin-like growth factor-1 (IGF-1) is an important regulator of cardiomyocyte homeostasis and cardiac structure, and the prosurvival and antiapoptotic effects of IGF-1 have been investigated. However, the effect of microRNA-320 (miR-320) in ischemia and reperfusion (I/R) by targeting IGF-1 is rarely discussed. We investigated the role of miR-320 in I/R injury. A total of 192 healthy female Wistar rats were divided into eight groups (n = 24). Rat heart I/R model was established. Hemodynamics, infarct size weight (ISW), heart function, and rat cardiomyocyte apoptosis were measured. Hypoxia-reoxygenation (H/R) in rat cardiomyocyte was used to simulate the I/R process. The mRNA levels of miR-320 and IGF-1, and proteins levels of IGF-1, IGF-1R, p-IGF-1R, p-ASK1, p-JNK, p-p38, Bcl-2, Bax and Caspase-3 were measured. In vivo inhibition of miR-320 expression significantly increased IGF-1 and IGF-1R mRNA levels, elevated the absolute values of SBP, DBP, MAP, ± dp/dtmax, LVEF and LVFS, decreased ISW, LVESD and LVEDd and the number of TUNEL positive cells, lowered the levels of p-ASK1, p-JNK, p-p38, Bax and Caspase-3 and increased expression of Bcl-2 compared to the I/R + NC group. Compared to H/R + NC group in vitro, miR-320 inhibition increased IGF-1 mRNA levels, inhibited cardiomyocyte apoptosis, down-regulated p-ASK, p-JNK, p-p38, Bax and Caspase-3 levels, and up-regulated Bcl-2 level. MiR-320 inhibition target elevated IGF-1 mRNA and protein levels, suppress early cardiomyocyte apoptosis of I/R, and inhibited ASK1-JNK/p38 pathway, which provides a new target for clinical study of I/R injury.

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MicroRNA-320a suppresses in GBM patients and modulates glioma cell functions by targeting IGF-1R

Cited by 55 publications

References 21 publications

MicroRNA-133a functions as a tumor suppressor by targeting IGF-1R in hepatocellular carcinoma

MicroRNA-133a functions as a tumor suppressor by targeting IGF-1R in hepatocellular carcinoma

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

Down-regulation of microRNA-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1

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