MicroRNA-378g enhanced radiosensitivity of NPC cells partially by targeting protein tyrosine phosphatase SHP-1

Lin, Ting; Zhou, Fulai; Zhou, Haibo; Pan, Xia; Sun, Ziyi; Peng, Gang

doi:10.3109/09553002.2015.1096028

Cited by 20 publications

(21 citation statements)

References 37 publications

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“…The radiosensitivity in NPC cells is also regulated by miRNAs. For instance, miR-24 [11,12] and miR-378g [13] can enhance the radiosensitivity of NPC cells. This provides evidence for a new clinical therapy treatment for NPC that combines radiation therapy with miRNA regulation in order to enhance the effects of treatment.…”

Section: Introductionmentioning

confidence: 99%

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

et al. 2017

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The aim of the present study was to explore the mechanism through which miR-130a-3p affects the viability, proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC). Tissue samples were collected from the hospital department. NPC cell lines were purchased to conduct the in vitro and in vivo assays. A series of biological assays including MTT, Transwell, and wound healing assays were conducted to investigate the effects of miR-130a-3p and BACH2 on NPC cells. MiR-130a-3p was down-regulated in both NPC tissues and cell lines, whereas BACH2 was up-regulated in both tissues and cell lines. MiR-130a-3p overexpression inhibited NPC cell viability, proliferation, migration, and invasion but promoted cell apoptosis. The converse was true of BACH2, the down-regulation of which could inhibit the corresponding cell abilities and promote apoptosis of NPC cells. The target relationship between miR-130a-3p and BACH2 was confirmed. The epithelial–mesenchymal transition (EMT) pathway was also influenced by miR-130a-3p down-regulation. In conclusion, miR-130a-3p could bind to BACH2, inhibit NPC cell abilities, and promote cell apoptosis.

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Section: Introductionmentioning

confidence: 99%

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

et al. 2017

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“…miR-222 confers radioresistance in NPC cells. It is well established that certain miRNAs can regulate the radioresistance of cancer cells (11)(12)(13)17,18). Thus, the effect of miR-222 on NPC cell radioresistance was investigated.…”

Section: Mir-222 Overexpression Increased Cell Viability and Colony Fmentioning

confidence: 99%

“…Growing evidence supports the critical role of miRNAs in the progression of human cancers, where they function as either oncogenic miRNAs (oncomirs) or tumor suppressors through the regulation of cellular proliferation, differentiation and apoptosis (8)(9)(10). A number of studies have demonstrated that miRNAs are involved in cellular ionizing radiation (IR) responses through cell cycle regulation and the apoptosis signal pathway in several types of cancer, including NPC (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN

Chen

et al. 2017

Mol Med Report

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MicroRNA-222 (miR‑222) has been reported to be involved in the initiation, development and metastasis of tumors, as well as conferring resistance to chemotherapeutic drugs or radiotherapy in various types of cancer. However, the role and the underlying molecular mechanism of miR‑222 specifically in nasopharyngeal carcinoma (NPC) remains unclear. Thus, the biological function and underlying mechanism of in miR‑222 was investigated in NPC tissue specimens and cell lines. miR‑222 was upregulated in NPC tissues and malignant cell lines compared with adjacent normal samples and cell lines. miR‑222 upregulation significantly increased NPC cell proliferation, colony formation and cell apoptosis. Furthermore, miR‑222 upregulation conferred radioresistance. It was also confirmed that phosphatase and tensin homolog (PTEN) was a direct target for miR‑222 in NPC cells. Alteration of miR‑222 expression was demonstrated to regulate the phosphoinositide 3‑kinase/protein kinase B pathway in NPC cells. These results suggest that miR‑222 may act as an oncomir in NPC by targeting PTEN, and has potential as a therapeutic target in NPC.

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“…It is reasonable to infer that porcine miR-378/G shared some key function with human miR-378 g, e.g. regulation in cancer resistance [35]. So our results in functional analysis of ssc-miR-378/G might also provide some prospect on study about hsa-miR-378 g. In our investigation of the topically relevant literature, only one report was found describing a target gain related to an miRNA SNP the miRNA seed region modify mRNA targeting, cause loss and gain of targeting [33], and are associated with diseases [11,12].…”

Section: Discussionmentioning

confidence: 99%

Spontaneous single nucleotide polymorphism in porcine microRNA-378 seed region leads to functional alteration

Chai

Chen

Luo

et al. 2018

Bioscience, Biotechnology, and Biochemistry

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Sequence variation in a microRNA (miRNA) seed region can influence its biogenesis and effects on target mRNAs; however, in mammals, few seed region mutations leading to functional alterations have been reported to date. Here, we report the identification of a single nucleotide polymorphism (SNP) with functional consequence located in the seed region of porcine miR-378. In vitro analysis of this rs331295049 A17G SNP showed significantly up-regulated expression of the mature miR-378 (miR-378/G). In silico target prediction indicated that the SNP would modulate secondary structure and result in functional loss affecting >85% of the known target genes of the wild-type miR-378 (miR-378/A), and functional gain affecting >700 new target genes, and dual-luciferase reporter assay verified this result. This report of a SNP in the seed region of miR-378 leads to functional alteration and indicates the potential for substantive functional consequences to the molecular physiology of a mammalian organism.

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MicroRNA-378g enhanced radiosensitivity of NPC cells partially by targeting protein tyrosine phosphatase SHP-1

Abstract: MiR-378g enhanced radiosensitivity partially by targeting SHP-1 in NPC cells. Cell invasion was also partially inhibited by miR-378g, but the effect was not mediated by SHP-1.

Cited by 20 publications

References 37 publications

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN

Spontaneous single nucleotide polymorphism in porcine microRNA-378 seed region leads to functional alteration

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