Retracted Article: RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells <i>via</i> the posttranscriptional suppression of HGFR

Shi, Fan; Zhang, Yingbin; Wang, Juan; Su, Jin; Li, Zi; Wang, Tao

doi:10.1039/c9ra01785b

Cited by 2 publications

(1 citation statement)

References 28 publications

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“…Interestingly, a previous study indicates that miR-181d overexpression can sensitize GBM cells to chemotherapeutics by targeting MALT1 and NF-κB signaling pathway [ 15 ]. In contrast, miR-3681 was proposed as a negative regulator in the proliferation and migration of cervical cancer cells [ 16 ]. Since GBM is a type of cancers associated with aberrant activation of NF-κB pathway [ 1 , 15 ], investigating the micoRNA targets of HOXD-AS2 and its potential role in pathway could provide novel insights for therapeutic intervention.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA (lncRNA) HOXD-AS2 promotes glioblastoma cell proliferation, migration and invasion by regulating the miR-3681-5p/MALT1 signaling pathway

Zhong

Cai

2021

Bioengineered

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Glioblastoma (GBM) is the most lethal type of brain cancer. An increasing number of studies suggest that long non-coding RNAs (lncRNAs) are implicated in tumor progression. LncRNA HOXD‐AS2 was reported to be highly expressed in glioma and associated with glioma grade and poor prognosis. However, the molecular mechanism remains to be elucidated. In this study, we first analyzed differentially expressed lncRNAs in glioblastoma using RNA-seq dataset (156 GBM samples and 5 adjacent normal samples in TCGA (Cancer Genome Atlas) and GTEx (Genotype-Tissue Expression) database). HOXD-AS2 was found to be significantly up-regulated in GBM tissues, which was further confirmed in GBM patient tumor samples and GBM cell lines. Silencing HOXD-AS2 inhibited cell proliferation, migration and invasion, and promoted cell apoptosis. We further identified and validated miR-3681-5p as a target of HOXD-AS2, and miR-3681-5p was negatively regulated by HOXD-AS2. By negatively affecting miR-3681-5p, HOXD-AS2 could promote the expression of MALT1 to augment the aggressiveness of GBM cells. miR-3681-5p overexpression or MALT1 knockdown attenuated aggressiveness of GBM cells. Importantly, silencing HOXD-AS2 suppressed tumorigenesis of GBM cells in the xenograft mouse model. Collectively, our study clarified the role of miR-3681-5p/MALT1 axis underlying the oncogenic function of lncRNA HOXD-AS2 in GBM. Future work is required to study the mechanism by which HOXD-AS2 is upregulated in GBM cells, which can provide novel insights into therapeutic intervention for GBM treatment.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA (lncRNA) HOXD-AS2 promotes glioblastoma cell proliferation, migration and invasion by regulating the miR-3681-5p/MALT1 signaling pathway

Zhong

Cai

2021

Bioengineered

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Design, synthesis and biological evaluation of novel N-sulfonylamidine-based derivatives as c-Met inhibitors via Cu-catalyzed three-component reaction

Nan

Zhang

et al. 2020

European Journal of Medicinal Chemistry

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Retracted Article: RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR

Abstract: In this study, RNA-sequencing was used to investigate the differentially expressed miRNAs between cervical cancer tissues and matched adjacent non-tumor tissues.

Cited by 2 publications

References 28 publications

Long non-coding RNA (lncRNA) HOXD-AS2 promotes glioblastoma cell proliferation, migration and invasion by regulating the miR-3681-5p/MALT1 signaling pathway

Long non-coding RNA (lncRNA) HOXD-AS2 promotes glioblastoma cell proliferation, migration and invasion by regulating the miR-3681-5p/MALT1 signaling pathway

Design, synthesis and biological evaluation of novel N-sulfonylamidine-based derivatives as c-Met inhibitors via Cu-catalyzed three-component reaction

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