SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

Yang, Jun; Tian, Fang

doi:10.1111/jcmm.14762

Cited by 41 publications

(26 citation statements)

References 27 publications

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“…Additionally, lncRNA PVT1 could promote the progression of multiple diseases. [28][29][30] Our current research further confirmed these results, suggesting that lncRNA PVT1 could act as a pro-inflammatory agent. In addition, our study firstly found that PVT1 played a key role in the occurrence of renal fibrosis, which supplemented the biological function of PVT1.…”

Section: Discussionsupporting

confidence: 78%

“…39 Furthermore, PVT1 could modulate the proliferation and apoptosis of lens epithelial cells in diabetic cataract through regulation miR-214-3p/MMP2 axis. 30 Besides, it has been previously reported that miR-181a-5p could mediate the progression of renal fibrosis. 40 Our study was similar to these previous findings, further indicating that PVT1 knockdown inhibited the progression of renal fibrosis via sponging miR-181a-5p.…”

Section: Discussionmentioning

confidence: 99%

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<p>LncRNA PVT1 Suppresses the Progression of Renal Fibrosis via Inactivation of TGF-β Signaling Pathway</p>

Cao

Qin

Zhang

et al. 2020

DDDT

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Background: Renal fibrosis is a frequent pathway leading to end-stage kidney dysfunction. In addition, renal fibrosis is the ultimate manifestation of chronic kidney diseases (CKD). Long noncoding RNAs (lncRNAs) are known to be involved in occurrence of renal fibrosis, and lncRNA plasmacytoma variant translocation 1 (PVT1) has been reported to act as a key biomarker in renal diseases. However, the role of PVT1 in renal fibrosis remains unclear. Materials and Methods: HK-2 cells were treated with TGF-β1 to mimic renal fibrosis in vitro. Gene and protein expressions in HK-2 cells were measured by qRT-PCR and Western-blot, respectively. ELISA was used to test the level of creatinine (CR) and blood urea nitrogen (BUN) in serum of mice. Additionally, unilateral ureteral obstruction (UUO)-induced renal fibrosis mice model was established to investigate the effect of PVT1 on renal fibrosis in vivo. Results: PVT1 was upregulated in TGF-β1-treated HK-2 cells. In addition, TGF-β1-induced upregulation of α-SMA and fibronectin in HK-2 cells was significantly reversed by PVT1 knockdown. Meanwhile, PVT1 bound to miR-181a-5p in HK-2 cells. Moreover, miR-181a-5p directly targeted TGF-βR1. Furthermore, miR-181a-5p antagonist could significantly reverse the antifibrotic effect of PVT1 knockdown. Besides, knockdown of PVT1 notably attenuated the symptom of renal fibrosis in vivo. Conclusion: Knockdown of PVT1 significantly inhibited the progression of renal fibrosis in vitro and in vivo. Thus, PVT1 may serve as a potential target for the treatment of renal fibrosis.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

<p>LncRNA PVT1 Suppresses the Progression of Renal Fibrosis via Inactivation of TGF-β Signaling Pathway</p>

Cao

Qin

Zhang

et al. 2020

DDDT

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“…The ceRNA hypothesis suggests that lncRNA competitively binds with microRNAs through microRNA response elements (MREs) and inhibits the down-regulation of mRNA translation by miRNAs [12]. Moreover, the role of lncRNA-miRNA-mRNA ceRNA regulatory networks has been revealed in different diseases, such as chronic myeloid leukemia, cardiovascular diseases, diabetic cataract, and myocardial infarction [13][14][15][16], which might impact the prognosis of the diseases. However, on the basis of high-throughput sequencing and large samples, only a few literatures have reported the role of ceRNA in PAAD.…”

Section: Introductionmentioning

confidence: 99%

Identification of a competing endogenous RNA network associated with prognosis of pancreatic adenocarcinoma

et al. 2020

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Background Emerging evidence suggests that competing endogenous RNAs plays a crucial role in the development and progress of pancreatic adenocarcinoma (PAAD). The objective was to identify a new lncRNA-miRNA-mRNA network as prognostic markers, and develop and validate a multi-mRNAs-based classifier for predicting overall survival (OS) in PAAD. Methods Data on pancreatic RNA expression and clinical information of 445 PAAD patients and 328 normal subjects were downloaded from The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC) and Genotype-Tissue Expression (GTEx). The weighted correlation network analysis (WGCNA) was used to analyze long non-coding RNA (lncRNA) and mRNA, clustering genes with similar expression patterns. MiRcode was used to predict the sponge microRNAs (miRNAs) corresponding to lncRNAs. The downstream targeted mRNAs of miRNAs were identified by starBase, miRDB, miRTarBase and Targetscan. A multi-mRNAs-based classifier was develop using least absolute shrinkage and selection operator method (LASSO) COX regression model, which was tested in an independent validation cohort. Results A lncRNA-miRNA-mRNA co-expression network which consisted of 60 lncRNAs, 3 miRNAs and 3 mRNAs associated with the prognosis of patients with PAAD was established. In addition, we constructed a 14-mRNAs-based classifier based on a training cohort composed of 178 PAAD patients, of which the area under receiver operating characteristic (AUC) in predicting 1-year, 3-year, and 5-year OS was 0.719, 0.806 and 0.794, respectively. The classifier also shown good prediction function in independent verification cohorts, with the AUC of 0.604, 0.639 and 0.607, respectively. Conclusions A novel competitive endogenous RNA (ceRNA) network associated with progression of PAAD could be used as a reference for future molecular biology research.

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“…As the latest generation of gene sequencing technology develops and bioinformatics advances, more and more non-coding RNAs (ncRNAs) are considered to be related to various human tumor diseases [33]. For example, NCK1-AS1 participates in the occurrence and development of tumors by affecting the level of related proteins.…”

Section: Discussionmentioning

confidence: 99%

Down-regulating lncRNA LINC00485 inhibits the development of osteosarcoma by regulating miR-361-5p/Twist1 axis

Hu¹,

Luo²,

Zhou³

et al. 2020

Preprint

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Background: Mounting researches have established that long-chain non-coding RNA (lncRNA) and microRNA (miRNA) occupy an essential position in osteosarcoma development. The present study attempted to explicate the functional role and mechanism of LINC00485 and miR-361-5p in regulating the osteosarcoma progression.Methods: RT-PCR was employed to measure LINC00485 expression in osteosarcoma tissues and adjacent healthy tissues. Moreover, the correlation between LINC00485 expression and the clinicopathological indexes was analyzed. Further, the LINC00485 low-expressed cell model was constructed, and the CCK8 assay was employed to measure cell proliferation, followed by the flow cytometry in apoptosis testing. Besides, Transwell assay was utilized to detect cell migration and invasion ability, and Western blot examined the alternations of epithelial mesenchymal transition (EMT) marker molecules (E-cadherin and Vimentin). Furthermore, bioinformatics analysis was taken advantage of predicting the downstream molecular targets of LINC00485. RT-PCR and Western blot were carried out respectively to estimate the expression variations of miR-361-5p and Twist1. Dual luciferase activity assay and RNA co-precipitation (RIP) assay were conducted to verify the targeting relationship between LINC00485 and miR-361-5p, miR-361-5p and Twist1.Results: In comparison with normal adjacent tissues, the LINC00485 expression in cancer tissues was profoundly up-regulated. LINC00485 low expression greatly attenuated proliferation, migration, invasion, and EMT in osteosarcoma cells, while enhancing apoptosis. Bioinformatics analysis claimed that miR-361-5p was a sponge miRNA for LINC00485, targeting the Twist1 expression. Further gain- and loss-experiments declared that miR-361-5p limited the osteosarcoma development by inhibiting osteosarcoma cell proliferation, metastasis and promoting apoptosis.Conclusions: LINC00485 acted as an oncogene in the osteosarcoma tumorigenesis by modulating the miR-361-5p/Twist1 axis.

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SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

Cited by 41 publications

References 27 publications

<p>LncRNA PVT1 Suppresses the Progression of Renal Fibrosis via Inactivation of TGF-β Signaling Pathway</p>

<p>LncRNA PVT1 Suppresses the Progression of Renal Fibrosis via Inactivation of TGF-β Signaling Pathway</p>

Identification of a competing endogenous RNA network associated with prognosis of pancreatic adenocarcinoma

Down-regulating lncRNA LINC00485 inhibits the development of osteosarcoma by regulating miR-361-5p/Twist1 axis

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