MiR‐24‐3p enhances cell growth in hepatocellular carcinoma by targeting metallothionein 1M

Dong, Xiaogang; Ding, Wei; Ye, Jianwei; Dong, Yan; Xue, Feng; Xu, Lin; Yin, Jiwei; Guo, Wenjia

doi:10.1002/cbf.3213

Cited by 27 publications

(29 citation statements)

References 29 publications

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“…To further explore the exactly regulated process of CASC2 in HCC, it was inferred that miR‐24‐3p may be the downstream target of CASC2 based on the published studies and bioinformatic analysis. Emerging studies indicated that miRNA, belongs to ncRNA, is also plays a crucial role in human HCC, including miR‐24‐3p . MiR‐24‐3p was up‐regulated in HCC tissues and serum, and promoted cell growth, which was correlated with poor prognosis of patients .…”

Section: Discussionmentioning

confidence: 99%

“…Emerging studies indicated that miRNA, belongs to ncRNA, is also plays a crucial role in human HCC, including miR‐24‐3p . MiR‐24‐3p was up‐regulated in HCC tissues and serum, and promoted cell growth, which was correlated with poor prognosis of patients . The direct or indirect modulation of miRNA by lncRNA is one of the important mechanisms to exert it biological function.…”

Section: Discussionmentioning

confidence: 99%

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LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR‐24‐3p

Fan

Zeng

et al. 2018

J of Cellular Biochemistry

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Cancer susceptibility candidate 2 (CASC2), a recently discovered long non-coding RNA (lncRNA), was confirmed to play numerous roles in several human cancers. However, the involvement and concrete mechanism of CASC2 in hepatocellular carcinoma (HCC) still need to be further elucidated. The relative expressions of CASC2 and miR-24-3p in HCC tissue and cell lines were determined by quantitative real-time PCR (qRT-PCR). The effects of CASC2 and miR-24-3p on HCC cells were further assessed via cell viability and apoptosis. In vivo tumorigenesis assay was performed to verify the inhibition effect of CASC2 on the tumor growth and further clarify the important role of miR-24-3p in this mechanism. Compared with the paired normal tissues, the relative expression of CASC2 significantly reduced in the HCC tissues, while miR-24-3p as determined by qRT-PCR obviously increased in the HCC tissues. This observation was also found in HCC cell lines. Meanwhile, the expression of CASC2 was negatively related to miR-24-3p expression in the HCC tissues (r = -0.804, P < 0.001). CASC2 could negatively regulate the expression of miR-24-3p in vitro. Moreover, CASC2 overexpression resulted in the growth inhibitory and apoptosis-inducing effects on HCC cells, but the up-regulation of miR-24-3p greatly eliminated the CASC2-induced effects. The tumorigenesis of HCC cells was restrained significantly by CASC2 overexpression as shown by decreased tumor volume and growth rate. However, miR-24-3p up-regulation rescued the inhibition of CASC2 on the tumor growth in tumor-bearing mice. LncRNA CASC2 inhibited the viability and induced the apoptosis of HCC cells through regulating miR-24-3p.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR‐24‐3p

Fan

Zeng

et al. 2018

J of Cellular Biochemistry

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“…Ding J, et al reported that low MT1M expression correlated with tumor recurrence and disease-free survival [33]. Dong X, et al reported that MT1M was downregulated in HCC tumor tissues significantly and miR-24-3p/MT1M pathway may contribute to the initiation and progression of HCC [34]. Ji XF, et al reported that MT1M promoter methylation was significantly increased in HCC group and was positively correlated with HCC tumor size [35].…”

Section: Discussionmentioning

confidence: 99%

Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma

Pan

et al. 2017

Oncotarget

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Members of the metallothionein (MT) family are involved in metal detoxifcation and in the protection of cells against certain electrophilic carcinogens. In present study, it was found that MT1M was downregulated in more than 77.1% (91/118) of hepatocellular carcinoma (HCC) tissues compared with adjacent non-tumor tissues. Furthermore, overexpression of MT1M inhibited cell viability, colony formation, cell migration and invasion in HCC cell lines and tumor cell growth in xenograft nude mice, and activated cell apoptosis in HCC cell lines. In addition, immunohistochemistry analysis showed MT1M was negative or weak staining in tumor tissues but moderate or strong staining in adjacent non-tumor tissues. The sensitivity and specificity of MT1M for HCC diagnosis were 76.27% and 89.83%, respectively. In conclusion, MT1M was identified as a potential tumor marker for HCC and may serve as a useful therapeutic agent for HCC gene therapy.

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“…Interestingly, miR‐24 and miR‐509 were significantly regulated in CAP‐mAb‐miR‐3074. miR‐24 is a well‐known proliferation enhancing oncogenic miRNA playing a crucial role in many different cancers (Chen et al, ; Dong et al, ; Hiller, Ovalle, Gagnon, Curran, & Wang, ; Zhang, Duan et al, ). In addition, miR‐509 has been shown to have anti‐proliferative effects in different cell lines (Wang et al, ; Wang, Deng, & Fu, ; Zhang, Liu, Han, Wang, & Yang, ).…”

Section: Discussionmentioning

confidence: 99%

Stable miRNA overexpression in human CAP cells: Engineering alternative production systems for advanced manufacturing of biologics using miR‐136 and miR‐3074

Weis

Guth

Fischer

et al. 2018

Biotech & Bioengineering

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Chinese hamster ovary (CHO) cells still represent the major production host for therapeutic proteins. However, multiple limitations have been acknowledged leading to the search for alternative expression systems. CEVEC's amniocyte production (CAP) cells are human production cells demonstrated to enable efficient overexpression of recombinant proteins with human glycosylation pattern. However, CAP cells have not yet undergone any engineering approaches to optimize process parameters for a cheaper and more sustainable production of biopharmaceuticals. Thus, we assessed the possibility to enhance CAP cell production capacity via cell engineering using miRNA technology. Based on a previous high-content miRNA screen in CHO-SEAP cells, selected pro-productive miRNAs including, miR-99b-3p, 30a-5p, 329-3p, 483-3p, 370-3p, 219-1-3p, 3074-5p, 136-3p, 30e-5p, 1a-3p, and 484-5p, were shown to act pro-productive and product independent upon transient transfection in CAP and CHO antibody expressing cell lines. Stable expression of miRNAs established seven CAP cell pools with an overexpression of the pro-productive miRNA strand. Subsequent small-scale screening as well as upscaling batch experiments identified miR-136 and miR-3074 to significantly increase final mAb concentration in CAP-mAb cells. Transcriptomic changes analyzed by microarrays identified several lncRNAs as well as growth and apoptosis-related miRNAs to be differentially regulated in CAP-mAb-miR-136 and -miR-3074. This study presents the first engineering approach to optimize the alternative human expression system of CAP-cells.

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MiR‐24‐3p enhances cell growth in hepatocellular carcinoma by targeting metallothionein 1M

Cited by 27 publications

References 29 publications

LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR‐24‐3p

LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR‐24‐3p

Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma

Stable miRNA overexpression in human CAP cells: Engineering alternative production systems for advanced manufacturing of biologics using miR‐136 and miR‐3074

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