The Oncogenic and Tumor Suppressive Functions of the Long Noncoding RNA MALAT1: An Emerging Controversy

Chen, Qingjuan; Zhu, Chenjing; Jin, Yingying

doi:10.3389/fgene.2020.00093

Cited by 65 publications

(66 citation statements)

References 81 publications

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“…While the study was performed in a different cancer model, the results are exactly opposite of ours. It looks like that MALAT1 might have different effects in different cancers but still such contrasting observations 38 make it important to comprehensively evaluate the role of MALAT1 before advancing the findings further in the clinics.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 facilitates lung metastasis of osteosarcomas through miR-202 sponging

Zhang

Piao

Ding

2020

Sci Rep

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Lungs are the primary metastatic sites for osteosarcomas responsible for associated mortality. Recent data has documented role of long non-coding RNAs (lncRNAs) in proliferation and growth of osteosarcoma cells. We evaluated a role of lncRNAs in the lung metastasis of osteosarcoma with the goal of identifying a unique signature. Comparison of different lncRNAs in tumor samples from osteosarcoma with and without lung metastasis led to identification of MALAT1 as the most differentially upregulated lncRNA in the osteosarcoma patients with lung metastasis. MALAT1 was also high in osteosarcoma cells KRIB and MALAT1’s targeted downregulation in these cells led to decreased invasive potential and identification of miR-202 as the miRNA that is sponged by MALAT1. In the lung metastasis in vivo model, parental KRIB cells metastasized to lungs and such metastasis was significantly inhibited in KRIB cells with downregulated MALAT1. Ectopic miR-202 expression attenuated KRIB downregulation-mediated effects on lung metastasis. In yet another in vivo model involving parental SAOS-2 and lung-metastatic derivatives SAOS-2-LM, MALAT1 expression was found to be elevated in lung metastatic cells, which also correlated with reduced miR-202. In conclusion, MALAT1-miR-202 represents a potential lncRNA-miRNA signature that affects lung metastasis of osteosarcomas and could potentially be targeted for therapy.

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Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 facilitates lung metastasis of osteosarcomas through miR-202 sponging

Zhang

Piao

Ding

2020

Sci Rep

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“…Recent studies suggest that lncRNAs are emerging as important regulators of cancer initiation, maintenance, and progression, attracting great attention. 14 Many dysregulated lncRNAs have been identified in human cancers, such as the well-characterized MALAT1, 15 H19 16 , HOTAIR, 17 and ANRIL 18 and so on. In the present study, we found a breast cancer-related lncRNA, IGF2-AS, which was significantly decreased in human breast cancer tissues, cells, as well as plasma.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA IGF2-AS represses breast cancer tumorigenesis by epigenetically regulating IGF2

Zhang¹,

Yan

Jiang

et al. 2020

Exp Biol Med (Maywood)

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Long non-coding RNAs are a kind of endogenous ncRNAs with a length of more than 200 bp. Accumulating evidence suggests that long non-coding RNAs function as pivotal regulators in tumorigenesis and progression. However, their biological roles in breast cancer remain largely unknown. Here, we found that IGF2 antisense RNA (IGF2-AS) was significantly decreased in breast cancer tissues, cell lines, and plasma. Patients with low IGF2-AS were more likely to develop larger tumor size and later clinical stage. Overexpression of IGF2-AS evidently inhibited the proliferation and induced apoptosis of MCF-7 and T47D cells in vitro, as well as retarded tumor growth in vivo. Further investigation revealed that IGF2-AS inhibited the expression of its sense-cognate gene IGF2 in an epigenetic DNMT1-dependent manner, resulting in the inactivation of downstream oncogenic PI3K/AKT/mTOR signaling pathway. Enforced expression of IGF2 could significantly block the tumor inhibitory effect of IGF2-AS. Importantly, we found that IGF2-AS could be used as an effective biomarker for breast cancer diagnosis and prognosis. Taken together, our study indicates that IGF2-AS is a tumor suppressor in breast cancer, restoration of IGF2-AS may be a promising treatment for this fatal disease.

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“…Furthermore, functional experiments both in vivo and in vitro demonstrated that lnc-HSD17B11-1:1 significantly promoted proliferation and metastatic abilities of CRC cells, while knockdown of lnc-HSD17B11-1:1 showed an inverse effect. A growing body of research suggests that some lncRNAs could serve as sponges for miRNAs to regulate the expression of target mRNA in CRC (Chen et al, 2020a). For instance, LINC00461 may be an oncogene in CRC by targeting miR-323b-3p through NFIB signaling pathway (Yu et al, 2019), Moreover, lncRNA MIR4435-2HG was reported to play an oncogenic role by promoting CRC growth and metastasis and establish the presence of MIR4435-2HG/miR-206/YAP1 axis in CRC (Dong et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Lnc-HSD17B11-1:1 Functions as a Competing Endogenous RNA to Promote Colorectal Cancer Progression by Sponging miR-338-3p to Upregulate MACC1

Zhang

Wang

et al. 2020

Front. Genet.

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Background: Long non-coding RNAs (lncRNAs) play pivotal roles in various kinds of human diseases, especially in cancer. However, regulatory role, clinical significance and underlying mechanisms of lncRNAs in colorectal cancer (CRC) liver metastasis still remain largely unknown. This study aimed to report a novel lncRNA, lnc-HSD17B-11:1, and its functional role in CRC progression. Materials and methods: Differentially expressed lnc-HSD17B11-1:1 was screened and identified from a lncRNA profile microarray. Quantitative real-time PCR was used to determine the expression levels and prognostic values of lncRNA in CRC cohorts. In vitro and in vivo functional experiments were performed to investigate the effects of lnc-HSD17B11-1:1 on tumor growth and metastasis in CRC. Mechanistically, Base Scope, bioinformatics analyses, dual luciferase reporter assay and RNA immunoprecipitation experiments were performed to confirm the association of lnc-HSD17B11-1:1 and miR-338-3p. Dual luciferase reporter assay, qRT-PCR and western blot analysis were performed to assess the relationships among lnc-HSD17B11-1:1, miR-338-3p, and MACC1. Results: Evidently up-regulation of lnc-HSD17B11-1:1 in CRC primary tissues was correlated with the depth of invasion (p = 0.043), clinical stage (p = 0.027), distant metastasis (p = 0.003) and poor prognosis of patients with CRC. lnc-HSD17B11-1:1 promoted CRC cell proliferation, mobility and invasion in vitro and in vivo. Mechanistic analysis revealed that lnc-HSD17B11-1:1 may act as a competing endogenous RNA (ceRNA) by acting as a sponge for miR-338-3p to upregulate the expression of MACC1. Conclusion: These findings suggest that lnc-HSD17B11-1:1 promotes CRC progression through lnc-HSD17B11-1:1/miR-338-3p/MACC1 axis and this might serve as a new diagnostic marker or target for treatment of CRC.

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The Oncogenic and Tumor Suppressive Functions of the Long Noncoding RNA MALAT1: An Emerging Controversy

Cited by 65 publications

References 81 publications

LncRNA MALAT1 facilitates lung metastasis of osteosarcomas through miR-202 sponging

LncRNA MALAT1 facilitates lung metastasis of osteosarcomas through miR-202 sponging

Long non-coding RNA IGF2-AS represses breast cancer tumorigenesis by epigenetically regulating IGF2

Lnc-HSD17B11-1:1 Functions as a Competing Endogenous RNA to Promote Colorectal Cancer Progression by Sponging miR-338-3p to Upregulate MACC1

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