LINC00520 targeting miR‐27b‐3p regulates <i>OSMR</i> expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway

Tian, Xiufen; Ji, Yongqiang; Liang, Yafeng; Zhang, Jing; Guan, Lina; Wang, Chunting

doi:10.1002/jcp.28118

Cited by 59 publications

(49 citation statements)

References 42 publications

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“…It was recently discovered that lncRNAs functioned as miRNA sponges. Tian's study indicated that lncRNA LINC00520 acted as a ceRNA to competitively inhibit miR-27b-3p during I/R injury 16 . Negative regulation between miR-21 and GAS5 was first found in breast tumors 12 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA GAS5 promotes apoptosis as a competing endogenous RNA for miR-21 via thrombospondin 1 in ischemic AKI

et al. 2020

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Mounting evidence has indicated that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) played important roles in renal ischemia/reperfusion (I/R) injury. However, the involvement of lncRNA growth arrest specific 5 (GAS5) in acute kidney injury (AKI) remained largely unexplored. This study aimed to determine possible mechanisms of GAS5 in the renal I/R process. We found that GAS5, noticeably upregulated by renal I/R injury, was further suppressed by delayed IPC while knockdown of miR-21 in vivo before IPC could significantly increased the GAS5 levels. Concurrently, TSP-1 was negatively regulated by miR-21 in vivo and vitro. Additionally, Reciprocal repression of GAS5 and miR-21 was identified. Knockdown of miR-21 in H6R0.5 treated HK-2 cells promoted apoptosis. Co-transfection of miR-21 mimic and pcDNA-GAS5 or pcDNA-Vector were performed, results of which showed that inhibition of miR-21 on TSP-1 could be rescued by overexpression of GAS5. This study suggested that GAS5 facilitated apoptosis by competitively sponging miR-21, which negatively regulated TSP-1 in renal I/R injury. This novel regulatory axis could act as a therapeutic target for AKI in the future.

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Section: Discussionmentioning

confidence: 99%

LncRNA GAS5 promotes apoptosis as a competing endogenous RNA for miR-21 via thrombospondin 1 in ischemic AKI

et al. 2020

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“…Pi3K/akt/mTor is a crucial signaling pathway involved in the carcinogenicity and tumorigenesis of different cancer types, and is closely related to cell biological functions, such as energy metabolism, proliferation, apoptosis and cell invasion (16)(17)(18)(19). Previous studies have revealed that certain mrnas are co-expressed with cYP2e1 and participate in the Pi3K/akt/mTor signaling pathway (20,21).…”

Section: Cyp2e1 Regulates Key Pi3k/akt/mtor Signaling Proteinsmentioning

confidence: 99%

CYP2E1 changes the biological function of gastric cancer cells via the PI3K/Akt/mTOR signaling pathway

et al. 2019

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The present study investigated the role of cytochrome P450 family 2 subfamily e polypeptide 1 (cYP2e1) in the development and progression of gastric cancer (Gc). The expression levels of cYP2e1 in MGc-803 Gc cells and normal GeS-1 cells were investigated via western blotting, and it was identified that the expression of CYP2E1 was different between GeS-1 and MGc-803 cells. cYP2e1 was overexpressed in MGc-803 cells using a lentiviral vector GV358. cell counting Kit-8, flow cytometry, cell migration and Matrigel invasion assays suggested that overexpression of cYP2e1 promoted the proliferation and invasion, and inhibited the apoptosis of Gc cells. The relationship between cYP2e1 expression and key signaling molecules in the Pi3K/akt/mTor signaling pathway was assessed. reverse transcription-quantitative Pcr analysis showed that mTor mrna expression was significantly increased after overexpression of cYP2e1 (P<0.05). Western blotting results showed that overexpression of cYP2e1 upregulated the expression of phosphorylated (p)-akt, p-mTor and p-p70 ribosomal protein S6 kinase (P70S6K; Ser371) proteins (P<0.05). To further investigate the relationship between cYP2e1 and the Pi3K/akt/mTor signaling pathway in Gc cells, MGc-803 cells were treated with the Pi3K inhibitor lY294002, and changes in the expression levels of Pi3K, aKT, mTor, P70S6K and cYP2e1 were observed. The present results showed that lY294002 downregulated the expression of Pi3K, cYP2e1, aKT, mTor and P70S6K (P<0.05). Therefore, changes in the biological function of Gc cells induced by cYP2e1 overexpression may be via the Pi3K/akt/mTor signaling pathway.

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“…Increasing evidences suggest miRNAs play a crucial role in occurrence and development of diseases. For renal I/R injury, miRNAs play an important role in different aspects, such as apoptosis and inflammation [18,19]. Xie et al reported that miR-128-3p improved the acute kidney injury via inhibiting cell apoptosis [18].…”

Section: Discussionmentioning

confidence: 99%

Mir10a overexpression aggravates the renal ischemia-reperfusion injury associated with a decrease in PIK3CA

Zhang

et al. 2020

Preprint

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Abstract Background: To investigate the effect of miR-10a on the renal tissues with ischemia-reperfusion (I/R) injury in rats and explore the underlying mechanisms of miR-10a in the HK-2 cells of hypoxia-reoxygenation. Methods: The miR-10a level was measured in renal tissues with I/R rats by RT-PCR. In order to research the role of miR-10a in the renal tissues, miR-10 agonist and miR-10a antagonist were used to treat I/R rats. The levels of serum creatinine (Scr) and blood urea nitrogen (BUN) in serum, renal histopathology, apoptosis of cells in renal tissues were analyzed, separately. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway related proteins were measured by Western blot. The HK-2 cell was cultured to study the mechanism of miR-10a in the model of hypoxia-reoxygenation. The dual luciferase reporter gene assay was used to confirm the PI3K p100 catalytic subunit α (PIK3CA) was a target gene of miR-10a. Results: After renal I/R injury in rats, the miR-10a expression was significantly increased (p<0.05). Injection of miR-10a agonist significantly aggravated the injury of renal and raised the apoptosis of cells in renal in rats with renal I/R injury (p<0.05). However, administration of miR-10a antagonist obviously improved the injury of renal, decreased the renal cells apoptosis and inhibited the PI3K/Akt pathway activity (p<0.05). In vitro experiments, the negative relation between PIK3CA and miR-10a was confirmed. Further, overexpression of miR-10a significantly decreased the proliferation of HK-2 cells, and increased the cells apoptosis via up-regulating PI3K/Akt pathway (p<0.05). Conclusion: miR-10a could aggravate the renal I/R injury associated with a decrease in PIK3CA/PI3K/Akt pathway.

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LINC00520 targeting miR‐27b‐3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway

Cited by 59 publications

References 42 publications

LncRNA GAS5 promotes apoptosis as a competing endogenous RNA for miR-21 via thrombospondin 1 in ischemic AKI

LncRNA GAS5 promotes apoptosis as a competing endogenous RNA for miR-21 via thrombospondin 1 in ischemic AKI

CYP2E1 changes the biological function of gastric cancer cells via the PI3K/Akt/mTOR signaling pathway

Mir10a overexpression aggravates the renal ischemia-reperfusion injury associated with a decrease in PIK3CA

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