Knockdown of long non-coding RNA MALAT1 increases the blood–tumor barrier permeability by up-regulating miR-140

Ma, Jun; Wang, Ping; Yao, Yilong; Liu, Yunhui; Li, Zhen; Liu, Xiaobai; Li, Zhiqing; Zhao, Xihe; Xi, Zhuo; Teng, Hao Wei; Liu, Jing; Xue, Yixue

doi:10.1016/j.bbagrm.2015.11.008

Cited by 67 publications

(57 citation statements)

References 69 publications

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“…It has been indicated in a recent study that lncRNAs have targeting relationships with miRNAs, which therefore regulates the expressions of target genes [11]. For instance, knockdown of lincRNA MALAT1 has been found increasing the blood-tumor barrier permeability by up-regulating miR-140, as supported by Ma et al [12] LncRNAs and miRNAs both play vital roles in several kinds of cancers, but the specific mechanism remains to be discussed. A complete understanding of the function of lncRNAs and miRNAs will contribute to novel therapeutic strategies.…”

Section: Introductionmentioning

confidence: 66%

Knockdown of Linc00515 Inhibits Multiple Myeloma Autophagy and Chemoresistance by Upregulating miR-140-5p and Downregulating ATG14

Yang

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The purpose of our experiments was to investigate the targeting relationship of linc00515, miR-140-5p and ATG14 and to explore the roles of linc00515, miR-140-5p and ATG14 in autophagy and chemoresistance of melphalan-resistant multiple myeloma cells. Methods: Plasmids that could interfere with the expression of linc00515 and ATG14 were loaded into myeloma cells, which were cultured with melphalan. MTT assay and flow cytometry analysis were utilized to investigate the effect of linc00515, miR-140-5p and ATG14 on the resistance of myeloma cells. QRT-PCR was used to determine the levels of mRNAs. Western blot was utilized to explore the level of ATG14 and autophagy-related proteins. Dual luciferase assay was utilized to explore the targeting relationship between linc00515, miR-140-5p and ATG14. GFP LC3 fluorescence assay was conducted to study the autophagy of cells. Results: The expression of linc00515 and ATG14 were significantly higher in melphalan-resistant myeloma cells. Knockdown of linc00515 and ATG14 led to decreased autophagy and chemoresistance of melphalan-resistant myeloma cells. The forced expression of miR-140-5p suppressed autophagy and chemoresistance of melphalan-resistant myeloma cells. Conclusion: Linc00515 enhanced autophagy and chemoresistance of melphalan-resistant myeloma by directly inhibiting miR-140-5p, which elevated ATG14 level.

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Section: Introductionmentioning

confidence: 66%

Knockdown of Linc00515 Inhibits Multiple Myeloma Autophagy and Chemoresistance by Upregulating miR-140-5p and Downregulating ATG14

Yang

Zhang

et al. 2018

Cell Physiol Biochem

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“…In addition, it has been reported that MALAT1 interacts with serine-/arginine-rich proteins to regulate the subcellular localization of proteins that regulate splicing (24). A recent study revealed that MALAT1 is critical for maintaining the blood-brain/blood-tumor barrier, which is characterized by the presence of tight junctions between brain capillary endothelial cells that restrict paracellular diffusion (25). This suggests that MALAT1 may regulate cerebral vascular endothelial barrier functions.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells

Xin

Jiang

2017

Experimental and Therapeutic Medicine

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Cerebral ischemia/reperfusion (I/R) injury leads to brain vascular dysfunction, which is characterized by endothelial cell injury or death. Long noncoding (lnc) RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is reportedly associated with endothelial cell functions and dysfunctions. In the present study, the role of MALAT1 in I/R-induced cerebral vascular endothelial cell apoptosis was explored using oxygen-glucose deprivation and reoxygenation (OGD-R) as an in vitro I/R injury model. Primary human brain microvascular endothelial cells were cultured under OGD-R, and the expression levels of MALAT1 and cell apoptosis were measured at 6, 9, 12, 24 and 36 h post-reoxygenation. The expression levels of MALAT1 and the apoptotic rate of cells exposed to OGD-R exhibited contrasting trends following reoxygenation. Following OGD-R, lentiviral overexpression of MALAT1 increased phosphatidylinositol 3-kinase (PI3K) activities and the activation of Akt phosphorylation, and decreased cell apoptosis and caspase 3 activities, which were successfully abolished by treatment with a PI3K inhibitor, Wortmannin. Conversely, lentiviral knockdown of MALAT1 decreased PI3K activities and the activation of Akt phosphorylation, and increased cell apoptosis and caspase 3 activity. Overexpression and knockdown of MALAT1 exhibited no significant effects on OGD-R-induced reactive oxygen species (ROS) production. In conclusion, to the best of our knowledge, the present study was the first to suggest that lncRNA MALAT1 may protect human brain vascular endothelial cells from OGD-R-induced apoptosis via a PI3K-dependent mechanism. These findings suggest that MALAT1 may be a potential novel therapeutic target for cerebral I/R injury.

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“…LncRNAs regulate gene expression epigenetically through competing for shared the miRNA response elements, therefore decreasing the binding of miRNA to its target genes [35–38]. Previous study showed that RMRP increased aggressive gastric cancer by regulating Cyclin D2 as the ceRNA for miR-206 [31].…”

Section: Discussionmentioning

confidence: 99%

LncRNA-RMRP Acts as an Oncogene in Lung Cancer

Meng

Ren

et al. 2016

PLoS ONE

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Accumulating studies have demonstrated that long noncoding RNAs (lncRNAs) act a crucial role in the development of tumors. However, the role of lncRNAs in lung cancer remains largely unknown. In this study, we demonstrated that theexpression of RMRP was upregulated in lung adenocarcinoma tissues compared to the matched adjacent normal tissues. Moreover, of 35 lung adenocarcinoma samples, RMRP expression was upregulated in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. We also showed that RMRP expression was upregulated in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE). Ectopic expression of RMRP promoted lung adenocarcinoma cell proliferation, colony formation and invasion. In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer. These data suggested that RMRP might serve as a therapeutic target in lung adenocarcinoma.

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Knockdown of long non-coding RNA MALAT1 increases the blood–tumor barrier permeability by up-regulating miR-140

Cited by 67 publications

References 69 publications

Knockdown of Linc00515 Inhibits Multiple Myeloma Autophagy and Chemoresistance by Upregulating miR-140-5p and Downregulating ATG14

Knockdown of Linc00515 Inhibits Multiple Myeloma Autophagy and Chemoresistance by Upregulating miR-140-5p and Downregulating ATG14

Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells

LncRNA-RMRP Acts as an Oncogene in Lung Cancer

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