Long non-coding RNA MALAT1 facilitates the tumorigenesis, invasion and glycolysis of multiple myeloma via miR-1271-5p/SOX13 axis

Liu, Na; Feng, Song; Li, Huanhuan; Chen, Xiaoguang; Bai, Songting; Liu, Yufeng

doi:10.1007/s00432-020-03127-8

Cited by 63 publications

(51 citation statements)

References 41 publications

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“…15,16 More importantly, a previous study indicated that MALAT1 could target miR-1271-5p to participate in the tumorigenesis of multiple myeloma. 17 However, the role and underlying mechanism of miR-1271-5p in DDP resistance of OC cells is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis</p>

Wang¹,

Han²,

Hu³

2020

CMAR

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Background: Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) were reported to be related to the development of ovarian cancer (OC). In this study, the functional mechanisms of lncRNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) and microRNA-1271-5p (miR-1271-5p) were explored in OC. Methods: The level of MALAT1, miR-1271-5p, or E2F transcription factor 5 (E2F5) was detected by qRT-PCR. MTT assay, flow cytometry analysis and transwell migration and invasion assays were performed to determine cell proliferation, apoptosis, migration and invasion, respectively. E2F5 protein expression was detected by Western blot. The interaction between miR-1271-5p and MALAT1 or E2F transcription factor 5 (E2F5) was confirmed by the dual-luciferase reporter assay. Results: MALAT1 and E2F5 level were increased, while miR-1271-5p level was decreased in cisplatin (DDP)-resistant OC tissues and cells. MALAT1 knockdown or miR-1271-5p upregulation decreased IC 50 of cisplatin, and inhibited cell proliferation, migration, invasion, and facilitated cell apoptosis in DDP-resistant OC cells. Moreover, MALAT1 sponged miR-1271-5p to upregulate E2F5 expression. Besides, MALAT1 knockdown decreased DDP resistance, inhibited cell proliferation, migration, invasion, and promoted cell apoptosis by sponging miR-1271-5p to downregulate E2F5 expression in DDP-resistant OC cell. Conclusion: We demonstrated that MALAT1 mediated DDP-resistant OC development through miR-1271-5p/E2F5 axis, providing the theoretical basis for OC therapy.

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Section: Introductionmentioning

confidence: 99%

<p>LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis</p>

Wang¹,

Han²,

Hu³

2020

CMAR

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“…At second, we probed into the mechanism of magnolol. It has been discovered that miR miR-342-3p and miR-124-3p are involved in suppression of MM [41][42][43][44][45][46]. The same results were also performed in detection of Cyclin D1, MMP-7 and MMP-9 protein expression levels through western blot.…”

Section: Discussionmentioning

confidence: 90%

Magnolol suppressed cell migration and invasion and induced cell apoptosis via inhibition of the NF-κB signaling pathway by upregulating microRNA-129 in multiple myeloma

Jin¹,

Wang²,

Zeng³

et al. 2021

neo

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Multiple myeloma (MM) is incurable cancer in the blood system. Magnolol is an effective component against various cancers. This study tried to investigate the effect and mechanism of magnolol on MM via regulating miR-129. Human normal plasma cells (nPCs) and MM cells U266 and LP1 were used in this study, accompanied by treatment of magnolol. The miR-129 inhibitor was transfected into U266 and LP1 cells during experiments. Cell viability was detected by Cell Counting Kit-8 assay. Cell migration and invasion were tested by wound healing assay and Transwell assay. And Annexin-V-FITC/PI assay was utilized to assess cell apoptosis. miR-129, miR-1271-5p, miR-342-3p, and miR-124-3p expressions were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and western blot was adopted to evaluate Cyclin D1, matrix metalloprotein (MMP)-7, MMP-9, phosphorylation (p)-p65, and p65 protein levels. In U266 and LP1 cells, with magnolol concentration increasing, cell viability, migration, and invasion rates, Cyclin D1, MMP-7, and MMP-9 expressions decreased, while cell apoptosis rose. And magnolol increased the miR-129 expression in MM cells. Besides, miR-129 inhibitor antagonized the above-mentioned effect of magnolol and partly offset the magnolol-induced decrease of p-p65 expression, as well as the ratio of p-p65 to p65 in U266 and LP1 cells. Magnolol suppressed cell migration and invasion and induced cell apoptosis via inhibiting NFpathway activation, by upregulating miR-129 in MM.

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“…For instance, LncRNA HOTAIRM1, which has dual properties as it interacts with both onco-suppressor and oncogenic miRs. HOTAIRM1 is located on human HOXA gene cluster and suggested to be involved in myeloid cell development [ 176 ]. A newly published article has shown the anti-tumor activity of lncRNA HOTAIRM1 by up-regulation of ARHGAP24 through miR-106a-5p inhibition [ 177 ].…”

Section: Microrna Ncrna and Zeb: Role In Emt And Cancer Metastasmentioning

confidence: 99%

MicroRNAs and Their Influence on the ZEB Family: Mechanistic Aspects and Therapeutic Applications in Cancer Therapy

et al. 2020

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Molecular signaling pathways involved in cancer have been intensively studied due to their crucial role in cancer cell growth and dissemination. Among them, zinc finger E-box binding homeobox-1 (ZEB1) and -2 (ZEB2) are molecules that play vital roles in signaling pathways to ensure the survival of tumor cells, particularly through enhancing cell proliferation, promoting cell migration and invasion, and triggering drug resistance. Importantly, ZEB proteins are regulated by microRNAs (miRs). In this review, we demonstrate the impact that miRs have on cancer therapy, through their targeting of ZEB proteins. MiRs are able to act as onco-suppressor factors and inhibit the malignancy of tumor cells through ZEB1/2 down-regulation. This can lead to an inhibition of epithelial-mesenchymal transition (EMT) mechanism, therefore reducing metastasis. Additionally, miRs are able to inhibit ZEB1/2-mediated drug resistance and immunosuppression. Additionally, we explore the upstream modulators of miRs such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), as these regulators can influence the inhibitory effect of miRs on ZEB proteins and cancer progression.

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Long non-coding RNA MALAT1 facilitates the tumorigenesis, invasion and glycolysis of multiple myeloma via miR-1271-5p/SOX13 axis

Cited by 63 publications

References 41 publications

<p>LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis</p>

<p>LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis</p>

Magnolol suppressed cell migration and invasion and induced cell apoptosis via inhibition of the NF-κB signaling pathway by upregulating microRNA-129 in multiple myeloma

MicroRNAs and Their Influence on the ZEB Family: Mechanistic Aspects and Therapeutic Applications in Cancer Therapy

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