MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells

Liu, Shikai; Song, Lili; Zeng, Saitian; Zhang, Liang

doi:10.1007/s13277-015-3732-4

Cited by 103 publications

(88 citation statements)

References 28 publications

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“…MALAT1 was reported to be an endogenous regulator of breast cancer progression by down-regulating miR-124 and activating the CDK4/E2F1 signaling pathway [23]. MALAT1 could modulate GRB2 expression via competing miR-124 to promote high-risk human papillomavirus (HR-HPV)-positive cervical cancer cell growth and invasion [30]. Here, our study further investigated whether MALAT1 could regulate apoptosis of DA neurons in PD by sponging miR-124.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA MALAT1 contributes to cell apoptosis by sponging miR-124 in Parkinson disease

et al. 2017

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BackgroundParkinson disease (PD) is the most common movement disturbance characterized by the loss of dopaminergic (DA) neurons in midbrain. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is aberrantly expressed in neurons and is involved in the dendritic and synapse development. However, the role of MALAT1 and its underlying mechanism in PD remain to be defined.MethodsThe expressions of MALAT1 and miR-124 were evaluated by qRT-PCR. N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice and SH-SY5Y cells subjected to N-methyl-4-phenylpyridinium (MPP+) were utilized to investigate the effect of MALAT1 on PD. TUNEL assay was performed to detect apoptosis of DA neurons in PD mice. Flow cytometry analysis was carried out to measure apoptosis of SH-SY5Y cells. Caspase3 activity and Cleaved Caspase3 expression were tested by caspase3 assay kit and western blot, respectively. TargetScan software and luciferase reporter assay were used to explore the relationship between MALAT1 and miR-124.ResultsMALAT1 was up-regulated and miR-124 was down-regulated in MPTP-induced PD mice and MPP+-treated SH-SY5Y cells. MALAT1 knockdown attenuated MPTP-induced apoptosis of DA neurons in MPTP-induced PD mouse model. MALAT1 interacted with miR-124 to negatively regulate its expression. MALAT1 knockdown suppressed MPP+-induced apoptosis in SH-SY5Y cells, while miR-124 downregulation abrogated this effect. Moreover, MALAT1 knockdown improved miR-124 expression in MPTP/MPP+ induced models of PD.ConclusionsMALAT1 promotes the apoptosis by sponging miR-124 in mouse models of PD and in vitro model of PD, providing a potential theoretical foundation for the clinical application of MALAT1 against PD.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA MALAT1 contributes to cell apoptosis by sponging miR-124 in Parkinson disease

et al. 2017

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“…28 Similarly, MALAT1 is abundant in neurons and is implicated in the development and/or maintenance of synapses. 30 One study has also demonstrated that the knockdown of MALAT1 expression inhibited MPTP-induced apoptosis in SH-SY5Y cells and in DA neurons of PD mice. 30 One study has also demonstrated that the knockdown of MALAT1 expression inhibited MPTP-induced apoptosis in SH-SY5Y cells and in DA neurons of PD mice.…”

Section: Discussionmentioning

confidence: 99%

Administration of resveratrol improved Parkinson’s disease‐like phenotype by suppressing apoptosis of neurons via modulating the MALAT1/miR‐129/SNCA signaling pathway

Xia

Sui

Zhang

2018

J of Cellular Biochemistry

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Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in the pathogenesis of Parkinson’s disease (PD). In addition, resveratrol was shown to regulate the expression of MALAT1. Therefore, the objective of this study was to clarify the role of resveratrol in PD. During the study, luciferase assays were conducted to determine the effect of resveratrol on the transcription efficiency of MALAT1 promoter as well as the regulatory relationships among MALAT1, miR‐129, and SNCA. In addition, real‐time PCR, Western blot analysis, MTT and flow cytometry analyses were conducted to investigate the mechanism of resveratrol in PD. Furthermore, a PD mouse model was established to study the role of resveratrol in vivo. It was found that resveratrol increased the number of TH+ cells and the expression of miR‐129, while decreasing the expression of MALAT1 and SNCA. In addition, MALAT1 inhibited the expression of miR‐129, a negative regulator of SNCA, thus increasing the expression of SNCA. A further mechanistic study revealed that resveratrol inhibited MALAT1 expression by blocking the transcription of the MALAT1 promoter. Finally, MPTP treatment could decrease cell proliferation and increase cell apoptosis, while resveratrol could partly offset the effect of MPTP. In summary, the therapeutic effect of resveratrol in the treatment of PD can be attributed to its ability to modulate the MALAT1/miR‐129/SNCA signaling pathway.

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“…MiR-124, a major miRNA that is associated with cancer, exerts regulatory effects on various oncogenes and participates in signaling pathways that are closely associated with cancer growth [28–30]. miR-124 exerts tumor suppressive functions on cell proliferation in bladder cancer [31], breast cancer [32] and non-small cell lung cancer [33].…”

Section: Discussionmentioning

confidence: 99%

The miR-124-p63 feedback loop modulates colorectal cancer growth

et al. 2017

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Among the diverse co-regulatory relationships between transcription factors (TFs) and microRNAs (miRNAs), feedback loops have received the most extensive research attention. The co-regulation of TFs and miRNAs plays an important role in colorectal cancer (CRC) growth. Here, we show that miR-124 can regulate two isoforms of p63, TAp63 and ΔNp63, via iASPP, while p63 modulates signal transducers and activators of transcription 1 (STAT1) expression by targeting miR-155. Moreover, STAT1 acts as a regulator of CRC growth by targeting miR-124. Taken together, these results reveal a feedback loop between miRNAs and TFs. This feedback loop comprises miR-124, iASPP, STAT1, miR-155, TAp63 and ΔNp63, which are essential for CRC growth. Moreover, this feedback loop is perturbed in human colon carcinomas, which suggests that the manipulation of this microRNA-TF feedback loop has therapeutic potential for CRC.

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MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells

Cited by 103 publications

References 28 publications

Long non-coding RNA MALAT1 contributes to cell apoptosis by sponging miR-124 in Parkinson disease

Long non-coding RNA MALAT1 contributes to cell apoptosis by sponging miR-124 in Parkinson disease

Administration of resveratrol improved Parkinson’s disease‐like phenotype by suppressing apoptosis of neurons via modulating the MALAT1/miR‐129/SNCA signaling pathway

The miR-124-p63 feedback loop modulates colorectal cancer growth

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