Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

Yang, Xi; Huang, Hongming; Wang, Xinfeng; Liu, Haiyan; Liu, Hong; Lin, Zenghua

doi:10.1186/s12935-020-1118-1

Cited by 22 publications

(17 citation statements)

References 21 publications

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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: 92%

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

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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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Section: Discussionmentioning

confidence: 92%

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

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“…Moreover, the knockdown of LINC01234 increases miR-124-3p and suppresses GRB2 expression, resulting in a decrease of cell proliferation and the inhibition of MM growth. These results demonstrate that lncRNAs play an important role in the pathobiology of MM ( Table 1 ) [ 13 , 33 , 34 , 35 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 48 , 50 , 51 , 53 , 56 , 57 , 58 , 59 , 62 , 69 , 72 , 78 , 79 , 81 , 82 , 83 , 84 , 85 , 86 , 88 , 90 , 91 , 92 , 94 , 95 , 96 , 97 , 107 ].…”

Section: Role Of Lncrnas In the Pathobiology Of MMmentioning

confidence: 83%

“…However, an increasing number of studies in MM are showing that lncRNAs can regulate or can be regulated by more than one miRNA, such as H19 (H19 imprinted maternally expressed transcript), UCA1 (urothelial cancer associated 1) or OIP5-AS1 (OIP5 antisense RNA 1). Remarkably, there are cases like TUG1 (taurine up-regulated 1) and H19 that are associated with the regulation of the same miRNA, miR-29b-3p ( Table 1 ) [ 33 , 39 , 42 , 44 , 45 , 51 , 53 , 57 , 58 , 59 , 60 , 72 , 81 , 82 , 83 , 88 , 90 , 91 , 94 , 95 , 96 ]. These results highlight the relevance of the miRNA sponge function of lncRNAs in MM.…”

Section: Role Of Lncrnas In the Pathobiology Of MMmentioning

confidence: 99%

The Role of lncRNAs in the Pathobiology and Clinical Behavior of Multiple Myeloma

Carrasco‐Leon

Amundarain

Gómez-Echarte

et al. 2021

Cancers

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MM is a hematological neoplasm that is still considered an incurable disease. Besides established genetic alterations, recent studies have shown that MM pathogenesis is also characterized by epigenetic aberrations, such as the gain of de novo active chromatin marks in promoter and enhancer regions and extensive DNA hypomethylation of intergenic regions, highlighting the relevance of these non-coding genomic regions. A recent study described how long non-coding RNAs (lncRNAs) correspond to 82% of the MM transcriptome and an increasing number of studies have demonstrated the importance of deregulation of lncRNAs in MM. In this review we focus on the deregulated lncRNAs in MM, including their biological or functional mechanisms, their role as biomarkers to improve the prognosis and monitoring of MM patients, and their participation in drug resistance. Furthermore, we also discuss the evidence supporting the role of lncRNAs as therapeutic targets through different novel RNA-based strategies.

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“…A large amount of research has shown that lncRNAs play an important role in the transcription pattern and functioning of MM. For example, knockdown of lncRNA SNHG16 significantly inhibits the proliferation of MM cells, suggesting that SNHG16 is a new therapeutic target for MM (14). In addition, lncRNA NEAT1 is highly expressed in MM samples, and silencing this gene can enhance the effect of traditional chemotherapy (15).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA AL928768.3 inhibits multiple myeloma cell proliferation by inducing cell cycle arrest in G0/G1 phase

Shen¹,

Jiang²,

Cong³

et al. 2022

Ann Transl Med

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Background: Multiple myeloma (MM) is a B-lymphocyte-derived malignancy. It ranks as the second most common hematological malignancy, with relatively high morbidity and mortality. However, the molecular mechanisms of MM occurrence and development remain elusive. This study found that long noncoding RNA AL928768.3 (lncRNA AL) was abnormally expressed in MM samples. However, the effect and molecular mechanism of lncRNA AL on the occurrence and development of MM remains unclear. Methods: Bone marrow fluids of MM patients (n=54) and volunteers (n=13) were collected and CD138 + cells were isolated. The expression level of lncRNA AL in MM cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR), and the correlation between the expression level of lncRNA AL and the clinicopathological features of patients was analyzed. Lentiviral vectors targeting lncRNA AL knockdown were constructed and transfected into cells. After transfection, the effects of lncRNA AL knockdown on MM cell proliferation and the cell cycle were detected by the CCK-8 assay, clone formation assay, and flow cytometry. The effect of lncRNA AL knockdown on MM cell cycle-related proteins was detected by Western blot. In addition, tumorigenicity experiments were performed in nude mice to detect the effect of lncRNA AL knockdown on MM cell proliferation in vivo. Results: LncRNA AL was highly expressed in MM patient samples and cell lines, and was significantly correlated with the disease stage of patients. Knockdown of lncRNA AL significantly inhibited the proliferation and colony formation of MM cells and induced cell cycle arrest in G0/G1 phase. Western blot analysis showed that knockdown of lncRNA AL significantly inhibited the expression of CDK2 and cyclin D1 and promoted the expression of cyclin suppressor p21. Knockdown of lncRNA AL significantly inhibited the proliferation of MM cells in nude mice. Conclusions: LncRNA AL was highly expressed in MM patients. Knockdown of this gene significantly inhibited the proliferative ability of MM cells and induced cell cycle arrest in G0/G1 phase. Therefore, lncRNA AL may be a novel biological target molecule for the early diagnosis, treatment, and prognostic evaluation of MM patients.

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Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

Cited by 22 publications

References 21 publications

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

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

The Role of lncRNAs in the Pathobiology and Clinical Behavior of Multiple Myeloma

Knockdown of lncRNA AL928768.3 inhibits multiple myeloma cell proliferation by inducing cell cycle arrest in G0/G1 phase

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