MicroRNA-1246 enhances migration and invasion through CADM1 in hepatocellular carcinoma

Sun, Zhao; Meng, Changting; Wang, Shihua; Zhou, Na; Guan, Mei; Bai, Chunmei; Lu, Shan; Han, Qin; Zhao, Robert Chunhua

doi:10.1186/1471-2407-14-616

Cited by 90 publications

(77 citation statements)

References 28 publications

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“…This is not surprising, given that miRNAs are known to target multiple targets. For instance, and as mentioned above, miR‐1246 has also been reported to enhance aggressive cancer phenotype by targeting the tumor suppressor, CADM1 . We speculate that there may be other mRNAs/pathways that miR‐1246 targets to regulate cancer stemness in HCC.…”

Section: Discussionsupporting

confidence: 52%

“…miR‐1246 have also been found to promote angiogenesis by activating small mothers of decapentaplegic 1/5/8 signaling elicited by promyelocytic leukemia down‐regulation in endothelial cells . In HCC, miR‐1246 has been shown to enhance metastasis by targeting cell adhesion molecule 1 (CADM1), a tumor‐suppressor gene involved in cell‐cell interactions . Circulating miR‐1246 has also been recently shown to predict tumor recurrence and survival in HCC patients after liver transplantation .…”

Section: Discussionmentioning

confidence: 99%

“…(33) In HCC, miR-1246 has been shown to enhance metastasis by targeting cell adhesion molecule 1 (CADM1), a tumor-suppressor gene involved in cell-cell interactions. (34) Circulating miR-1246 has also been recently shown to predict tumor recurrence and survival in HCC patients after liver transplantation. (35) In contrast, miR-1246 expression was shown to be decreased in cervical cancer tissues (36) and to inhibit HCC cell growth by targeting nuclear factor I/B and in a p53-induced manner.…”

Section: Discussionmentioning

confidence: 99%

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Octamer 4/microRNA‐1246 signaling axis drives Wnt/β‐catenin activation in liver cancer stem cells

et al. 2016

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Octamer 4/microRNA‐1246 signaling axis drives Wnt/β‐catenin activation in liver cancer stem cells

et al. 2016

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“…Meanwhile, this study also demonstrated that miR-1246 induced secretion of key pro-inflammatory cytokines and chemokines (IL-6, CCL2 and CCL5) in MSCs was mediated via NF-κB signaling pathway [25]. At the functional level, miR-1246 had been shown to induce the proliferation, invasion and migration and enhance cell apoptosis of cervical or hepatocellular carcinoma cells [28, 29]. In our study, we found that our results were consistent with previous studies, that overexpression of miR-1246 strengthened the decrease in cell viability, the increase in apoptosis, and the overproduction of pro-inflammatory factors after LPS exposure.…”

Section: Discussionmentioning

confidence: 99%

MiR-1246 Promotes LPS-Induced Inflammatory Injury in Chondrogenic Cells ATDC5 by Targeting HNF4γ

Zhang

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Osteoarthritis (OA) is a common inflammatory joint disease. miRNAs are associated with OA and functionally implicated in the pathogenesis of the disease. In the present study, we investigated the role of miR-1246 in the lipopolysaccharide (LPS)-induced inflammatory injury of ATDC5 cells. Methods: ATDC5 cells were cultured and treated with LPS in a series of concentration (0, 1, 5, and 10 µg/ml) for 5 h. The cells were transfected with miR-1246-mimic, inhibitor, si-HNF4γ or negative control, then were assessed for cell viability using CCK8 assay, apoptosis by flow-cytometry and expressions of miR-1246 and pro-inflammatory cytokines by qRT-PCR and western blot analysis. Results: Cell viability was significantly reduced and cell apoptosis was added in ATDC5 cells injured with LPS at the dosage of 5 and 10 µg/ml. Relative mRNA expressions of pro-inflammatory cytokines (IL-1β, IL-6, IL-8 and TNF-α) were significantly increased. miR-1246 was up-regulated in ATDC5 cells treated with LPS. Moreover, miR-1246 overexpression aggravated LPS-induced decrease in cell viability, increase in apoptosis and overproduction of pro-inflammatory factors. mRNA and protein expressions of HNF4γ were significantly suppressed in cells transfected with miR-124-mimic. Further, miR-1246 knockdown alleviated LPS-induced inflammatory injury by up-regulating the expression of HNF4γ and activation of PI3K/AKT and JAK/STAT pathways. Conclusions: Suppression of miR-1246 alleviated LPS-induced inflammatory injury in chondrogenic ADTC5 cells by up-regulation of HNF4γ and activation of PI3K/AKT and JAK/STAT pathways. The findings of this study will provide a novel viewpoint regarding miR-1246 target for clinical.

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“…It has been reported that miR-1246 was an oncogenic miRNA linking with cancer migration and invasion [46], but there was no literature concerning the role of miR-1246 in radiosensitivity. Figure 3 shows that inhibition of miR-1246 in A549 cells bearing a high level of intrinsic miR-1246 significantly suppressed cell proliferation and increased cell radiosensitivity; while transfection of H446 cells with miR-1246 mimic promoted cell growth and enhanced cell radioresistance.…”

Section: Discussionmentioning

confidence: 99%

Extracellular miR-1246 promotes lung cancer cell proliferation and enhances radioresistance by directly targeting DR5

Yuan

Wang

et al. 2016

Oncotarget

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MiRNAs in the circulation have been demonstrated to be a type of signaling molecule involved in intercellular communication but little is known about their role in regulating radiosensitivity. This study aims to investigate the effects of extracellular miRNAs induced by ionizing radiation (IR) on cell proliferation and radiosensitivity. The miRNAs in the conditioned medium (CM) from irradiated and non-irradiated A549 lung cancer cells were compared using a microarray assay and the profiles of 21 miRNAs up and down-regulated by radiation were confirmed by qRT-PCR. One of these miRNAs, miR-1246, was especially abundant outside the cells and had a much higher level compared with that inside of cells. The expressions of miR-1246 in both A549 and H446 cells increased along with irradiation dose and the time post-irradiation. By labeling exosomes and miR-1246 with different fluorescence dyes, it was found that the extracellular miR-1246 could shuttle from its donor cells to other recipient cells by a non-exosome associated pathway. Moreover, the treatments of cells with miR-1246 mimic or its antisense inhibitor showed that the extracellular miR-1246 could enhance the proliferation and radioresistance of lung cancer cells. A luciferase reporter-gene transfer experiment demonstrated that the death receptor 5 (DR5) was the direct target of miR-1246, and the kinetics of DR5 expression was opposite to that of miR-1246 in the irradiated cells. Our results show that the oncogene-like extracellular miR-1246 could act as a signaling messenger between irradiated and non-irradiated cells, more importantly, it contributes to cell radioresistance by directly suppressing the DR5 gene.

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MicroRNA-1246 enhances migration and invasion through CADM1 in hepatocellular carcinoma

Cited by 90 publications

References 28 publications

Octamer 4/microRNA‐1246 signaling axis drives Wnt/β‐catenin activation in liver cancer stem cells

Octamer 4/microRNA‐1246 signaling axis drives Wnt/β‐catenin activation in liver cancer stem cells

MiR-1246 Promotes LPS-Induced Inflammatory Injury in Chondrogenic Cells ATDC5 by Targeting HNF4γ

Extracellular miR-1246 promotes lung cancer cell proliferation and enhances radioresistance by directly targeting DR5

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