microRNA-365-targeted nuclear factor I/B transcriptionally represses cyclin-dependent kinase 6 and 4 to inhibit the progression of cutaneous squamous cell carcinoma

Zhou, Liang; Wang, Yinghui; Ou, Chengshan; Lin, Zhixiang; Wang, Yunlong; Liu, Hongxia; Zhou, Meijuan; Ding, Zhenhua

doi:10.1016/j.biocel.2015.06.009

Cited by 27 publications

(36 citation statements)

References 34 publications

(46 reference statements)

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“…Thus, we screened and found that BAX was consistently predicted to be one of the downstream targets of miR-365 by web-based software, including TargetScan [13], miRanda [14], and miRDB [15]. Importantly, as a known apoptosis regulator, the role of BAX in CSCC tumorigenesis is underexplored.…”

Section: Resultsmentioning

confidence: 99%

“…Evidence also supports the role of miR-365 in the malignant transformation of keratinocytes, promoting the development of CSCC, and inhibition of miR-365 by antagomiR oligo treatment that can repress CSCC tumor formation in vivo [11,12]. The identified downstream targets of miR-365 include cell division cycle 25A (CDC25A), cyclin D1 (CCND1), transcription termination factor 1 (TTF1), interleukin 6 (IL-6) and nuclear factor I B (NFIB) in various types of cancers [13,14,15,16,17,18,19]. In view of the regulatory functions of microRNA are performed through targeting multiple downstream genes, it is necessary to investigate the important downstream targets to unveil all of the critical roles performed by this microRNA, which may also improve our understanding of mechanistic regulation of microRNAs in CSCC.…”

Section: Introductionmentioning

confidence: 99%

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Loss of BAX by miR-365 Promotes Cutaneous Squamous Cell Carcinoma Progression by Suppressing Apoptosis

Zhou

Gao

Wang

et al. 2017

IJMS

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Pro-apoptotic BCL2 associated X (BAX) is traditionally thought to be regulated by anti-apoptotic BCL-2 family members, like BCL2-like 1 (BCL-XL), at the protein level. However, the posttranscriptional regulation of BAX is under explored. In this study, we identified BAX as the novel downstream target of miR-365, which is supported by gain- and loss-of-function studies of onco-miR-365. Loss of BAX by either RNA interference or highly-expressed miR-365 in cells of cutaneous squamous cell carcinoma (CSCC) enhanced the tumor resistance against apoptosis, while repressing cell proliferation, migration, and invasiveness. In vivo experiment confirmed that BAX knockdown promotes the growth of CSCC xenografts. Collectively, our results find a miR-365-BAX axis for alleviating the pro-apoptotic effects of BAX, which promotes CSCC development and may facilitate the generation of novel therapeutic regimens to the clinical treatment of CSCC.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loss of BAX by miR-365 Promotes Cutaneous Squamous Cell Carcinoma Progression by Suppressing Apoptosis

Zhou

Gao

Wang

et al. 2017

IJMS

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“…1), also encodes an miRNA with known tumour suppressor function, as evidenced by its ability to target specific transcription factors, such as NKX2-1 and TTF1, in non-small cell lung cancer (Qi et al 2012; Kang et al 2013; Sun et al 2015). miR365 is down-regulated in colon cancer (Nie et al 2012), cutaneous squamous cell carcinoma (Zhou et al 2014, 2015), hepatocellular carcinoma (Chen et al 2015), gastric cancer (Guo et al 2013) and malignant melanoma (Bai et al 2015a, b). By contrast, putative tumour suppressor functions of the other two miRNAs located within the NF1 microdeletion region, encoded by MIR4725 and MIR4733, respectively, have not so far been reported.…”

Section: Co-deleted Genes With the Potential To Influence The Clinicamentioning

confidence: 99%

Emerging genotype–phenotype relationships in patients with large NF1 deletions

2017

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The most frequent recurring mutations in neurofibromatosis type 1 (NF1) are large deletions encompassing the NF1 gene and its flanking regions (NF1 microdeletions). The majority of these deletions encompass 1.4-Mb and are associated with the loss of 14 protein-coding genes and four microRNA genes. Patients with germline type-1 NF1 microdeletions frequently exhibit dysmorphic facial features, overgrowth/tall-for-age stature, significant delay in cognitive development, large hands and feet, hyperflexibility of joints and muscular hypotonia. Such patients also display significantly more cardiovascular anomalies as compared with patients without large deletions and often exhibit increased numbers of subcutaneous, plexiform and spinal neurofibromas as compared with the general NF1 population. Further, an extremely high burden of internal neurofibromas, characterised by >3000 ml tumour volume, is encountered significantly, more frequently, in non-mosaic NF1 microdeletion patients than in NF1 patients lacking such deletions. NF1 microdeletion patients also have an increased risk of malignant peripheral nerve sheath tumours (MPNSTs); their lifetime MPNST risk is 16–26%, rather higher than that of NF1 patients with intragenic NF1 mutations (8–13%). NF1 microdeletion patients, therefore, represent a high-risk group for the development of MPNSTs, tumours which are very aggressive and difficult to treat. Co-deletion of the SUZ12 gene in addition to NF1 further increases the MPNST risk in NF1 microdeletion patients. Here, we summarise current knowledge about genotype–phenotype relationships in NF1 microdeletion patients and discuss the potential role of the genes located within the NF1 microdeletion interval whose haploinsufficiency may contribute to the more severe clinical phenotype.

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“…For example, the interaction between H. pylori and the TLR4 gene and miR-146a polymorphisms has been studied. It was found that the combined effect of the miR-146a rs2910164 GG genotype and the TLR4 + 3725C allele could increase the risk of severe atrophic gastritis in a Japanese population infected with H. pylori 16. In addition, Song et al .…”

Section: Discussionmentioning

confidence: 98%

Association of Polymorphisms in three pri-miRNAs that Target Pepsinogen C with the Risk and Prognosis of Gastric Cancer

Wu¹,

Xu²,

et al. 2017

Sci Rep

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We aimed to explore the associations of polymorphisms in three microRNAs (miRNAs) (let-7e rs8111742, miR-365b rs121224 and miR-4795 rs1002765) that target PGC with the risk and prognosis of gastric cancer/atrophic gastritis. Sequenom’s MassArray was used to genotype the miRNA polymorphisms in 724 gastric cancer cases, 862 atrophic gastritis cases and 862 controls in a Chinese population. We found that let-7e rs8111742 and miR-4795 rs1002765 were associated with the risk of gastric cancer in the H. pylori-positive subgroup. MiR-365b rs121224 was associated with the risk of intestinal-type gastric cancer in the alcohol consumption subgroup. Intestinal-type gastric cancer patients at Borrmann stages III-IV who carry the miR-365b rs121224 GG genotype had better prognosis compared with those who carry the CG or CC genotypes. MiR-365b rs121224 was associated with Lauren typing and TNM staging, in which the distribution of GG genotype carriers in intestinal-type gastric cancer and the TNM stage I-II subgroup was higher than that of CG or CC genotypes, which contrasted with the distribution in diffuse-type gastric cancer or TNM III-IV groups. These findings suggested that the polymorphisms in these miRNAs might be biomarkers for gastric cancer risk and prognosis, especially for populations infected with Helicobacter pylori or who consume alcohol.

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microRNA-365-targeted nuclear factor I/B transcriptionally represses cyclin-dependent kinase 6 and 4 to inhibit the progression of cutaneous squamous cell carcinoma

Cited by 27 publications

References 34 publications

Loss of BAX by miR-365 Promotes Cutaneous Squamous Cell Carcinoma Progression by Suppressing Apoptosis

Loss of BAX by miR-365 Promotes Cutaneous Squamous Cell Carcinoma Progression by Suppressing Apoptosis

Emerging genotype–phenotype relationships in patients with large NF1 deletions

Association of Polymorphisms in three pri-miRNAs that Target Pepsinogen C with the Risk and Prognosis of Gastric Cancer

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