Requirement of miR-144 in CsA Induced Proliferation and Invasion of Human Trophoblast Cells by Targeting Titin

Liang, Ying; Lin, Qinlu; Luo, Feijun; Wu, Wei; Yang, Tao; Wan, Shumei

doi:10.1002/jcb.24710

Cited by 18 publications

(18 citation statements)

References 33 publications

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“…miRNAs function via base pairing with complementary sequences within mRNA molecules [20,21,22,23], cutting off the mRNA molecule on target genes, or inhibiting translation of target genes. Some research has indicated that miR-144 is downregulated in many cancers [24,25,26,27,28,29,30,31]. These previous findings coincide with our results, which identified that miR-144 is significantly downregulated in human lung cancer.…”

Section: Discussionsupporting

confidence: 92%

MiR-144 Inhibits Proliferation and Induces Apoptosis and Autophagy in Lung Cancer Cells by Targeting TIGAR

Chen

Li²,

Li³

et al. 2015

Cell Physiol Biochem

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Background: MiRNAs are noncoding RNAs of 20-24 nucleotides that function as post-transcriptional negative regulators of gene expression. MiRNA genes are usually transcribed by RNA polymerase II in the nucleus. Their initial products are pre-miRNAs which have cap sequences and polyA tails. The p53-induced glycolysis and apoptosis regulator (TIGAR) was discovered through microarray analysis of gene expression following activation of p53. However, little is known about the effect of miR-144 on cell proliferation and apoptosis and how it interacts with TIGAR. Methods: We performed real-time PCR, western blotting, CCK8, colony formation, tumor growth, flow cytometry, Caspase3/7 activity, Hoechst 33342 staining, MDC staining of autophagic cells and luciferase reporter assays to detect the influence of miR-144 to lung cancer cells. Results: miR-144 targeted TIGAR, inhibited proliferation, enhanced apoptosis, and increased autophagy in A549 and H460 cells. Conclusions: Our study improves our understanding of the mechanisms underlying lung cancer pathogenesis and may promote the development of novel targeted therapies.

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Section: Discussionsupporting

confidence: 92%

MiR-144 Inhibits Proliferation and Induces Apoptosis and Autophagy in Lung Cancer Cells by Targeting TIGAR

Chen

Li²,

Li³

et al. 2015

Cell Physiol Biochem

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“…In our previous study, Cyclosporin A (CsA) has been revealed to inhibit miR‐144 expression to regulate proliferation and invasion of human trophoblast (HT) cells through miR‐144 targeting titin [Liang et al, ]. We demonstrated the mechanism by which CsA promotes titin expression to increase the vitality of HT cells.…”

mentioning

confidence: 80%

“…Recently, Opitz et al [] showed evidence of a previously unknown isoform of titin, termed as N2BA‐1, and this novel isoform is dominant in the fetus and almost absent by birth in the rat. In our previous study, we demonstrated that miR‐144 could inhibit HT cells’ proliferation and invasion via direct targeting titin [Liang et al, ]. Thus, it is likely that titin expression may be involved in the process of placentation and embryo development.…”

mentioning

confidence: 97%

CsA Promotes XIST Expression to Regulate Human Trophoblast Cells Proliferation and Invasion Through miR-144/Titin Axis

Liang

Zhu

et al. 2017

J. Cell. Biochem.

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In our previous study, we revealed that Cyclosporin A (CsA) could inhibit miR-144 expression to regulate proliferation and invasion of human trophoblast (HT) cells through miR-144 targeting titin. This partially demonstrated the mechanism by which CsA promotes titin expression to increase the vitality of HT cells. However, the mechanism by which CsA inhibits miR-144 expression remains to be investigated. Recently, the interaction between lncRNA and miRNA has been frequently reported to play major role in several biological processes. In the present study, online tools were used to figure out that X-inactive specific transcript (XIST) could interact with miR-144. XIST and miR-144 reciprocally inhibited each other in HT cells; as exhibited by luciferase reporter gene assays, miR-144 bind to XIST by direct targeting. XIST suppressed miR-144 expression to promote titin expression. As exhibited by the Spearman's correlation analysis, in CsA treated HT cells, miR-144 was inversely correlated with titin and XIST, respectively; XIST was positively correlated with titin. Moreover, CsA could promote the proliferation and invasion of HT cells through XIST and the downstream MAPK and MMPs pathway. Taken together, these findings will shed light to the role and mechanism of CsA/XIST/miR-144/titin in regulating HT cells proliferation and invasion. XIST may serve as a potential therapeutic target in HT in the future. J. Cell. Biochem. 118: 2208-2218, 2017. © 2017 Wiley Periodicals, Inc.

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“…Two microRNAs—miR-19 and miR-574 have been reported to be related to CsA immunosuppression effect. miR-19 has been reported to be downregulated by CsA in vitro[18] while miR-574 has been reported to be downregulated with acute rejection in human [19]. MiR-15 has been reported to be lower in urine with glomerulosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Cyclosporine A alters expression of renal microRNAs: New insights into calcineurin inhibitor nephrotoxicity

et al. 2017

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Calcineurin inhibitors are powerful immunosuppressants that revolutionized organ transplantation. However, non-immune effects of the calcineurin inhibitor, such as cyclosporine A (CsA), have significantly hindered their use. Specifically, nephrotoxicity, which is associated with tubulointerstitial fibrosis, inflammation, and podocyte damage, affects up to half of all transplant patients. Calcineurin is involved in many aspects of kidney development and function; therefore, mechanisms of CsA-induced nephrotoxicity are complex and not yet fully understood. MicroRNAs are short non-coding RNAs that regulate protein-coding RNA expression through post-translational repression of target messenger RNAs. MicroRNA dysregulation is known to be involved in kidney diseases including fibrosis. In this study, we compared the renal microRNA expression profiles between mice that received CsA (20 mg/kg) or vehicle daily for six weeks. The results demonstrate that CsA induces significant changes in renal microRNA expression profile. We used combined criteria of False Discovery Rate (≤0.1), fold change (≥2) and median signal strength (≥50) and identified 76 differencially expressed microRNAs. This approach identified microRNAs previously linked to renal fibrosis that includes let-7d, miR-21, miR-29, miR-30, miR-130, miR-192, and miR-200 as well as microRNAs that have not been reported to be related to nephrotoxicity or immunosuppression. Pathway analysis of microRNA/mRNA changes highlights the Wnt, TGF-β, mTOR, and VEGF pathways. The mRNA expression profiles were compared in the same samples. The change of mRNA and microRNA profiles showed close correlations. To validate that the observed microRNA and mRNA expression level changes in mice kidney tissue were directly related to CsA treatment, the expression change induced by CsA treatment of three microRNAs (miR-21, miR-186, and miR-709) and three mRNAs (BMPR1a, SMURF1 and SMAD7) were compared in HEK293 cell line. A similar trend of expression level change was induced by CsA treatment in all selected microRNAs and mRNAs in the in vitro cell model. These data provide a roadmap for future work to study the role of the known and novel candidate microRNAs in the mechanism of nephrotoxicity and their further therapeutic potential.

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Requirement of miR-144 in CsA Induced Proliferation and Invasion of Human Trophoblast Cells by Targeting Titin

Cited by 18 publications

References 33 publications

MiR-144 Inhibits Proliferation and Induces Apoptosis and Autophagy in Lung Cancer Cells by Targeting TIGAR

MiR-144 Inhibits Proliferation and Induces Apoptosis and Autophagy in Lung Cancer Cells by Targeting TIGAR

CsA Promotes XIST Expression to Regulate Human Trophoblast Cells Proliferation and Invasion Through miR-144/Titin Axis

Cyclosporine A alters expression of renal microRNAs: New insights into calcineurin inhibitor nephrotoxicity

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