Circular RNA PRKCI promotes glioma cell progression by inhibiting microRNA-545

Zhang, Xuebang; Han, Yang; Li, Zhao; Li, Gang; Duan, Yuxia

doi:10.1038/s41419-019-1863-z

Cited by 31 publications

(19 citation statements)

References 40 publications

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“…OB-6 cells or primary osteoblasts were seeded into six-well plates (at a density of 3 × 10 5 cells per well). Following the applied DEX treatment cell apoptosis was tested by Annexin V-PI assay, using the described protocol 28 .…”

Section: Methodsmentioning

confidence: 99%

PGK1 depletion activates Nrf2 signaling to protect human osteoblasts from dexamethasone

et al. 2019

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Activation of nuclear-factor-E2-related factor 2 (Nrf2) cascade can alleviate dexamethasone (DEX)-induced oxidative injury and death of human osteoblasts. A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade. Here, in OB-6 osteoblastic cells and primary human osteoblasts, PGK1 silencing, by targeted shRNA, induced Nrf2 signaling cascade activation, causing Nrf2 protein stabilization and nuclear translocation, as well as increased expression of ARE-dependent genes (HO1, NQO1, and GCLC). Functional studies demonstrated that PGK1 shRNA largely attenuated DEX-induced oxidative injury and following death of OB-6 cells and primary osteoblasts. Furthermore, PGK1 knockout, by the CRISPR/Cas9 method, similarly induced Nrf2 signaling activation and protected osteoblasts from DEX. Importantly, PGK1 depletion-induced osteoblast cytoprotection against DEX was almost abolished by Nrf2 shRNA. In addition, Keap1 shRNA mimicked and nullified PGK1 shRNA-induced anti-DEX osteoblast cytoprotection. At last we show that PGK1 expression is downregulated in human necrotic femoral head tissues of DEX-taking patients, correlating with HO1 depletion. Collectively, these results show that PGK1 depletion protects human osteoblasts from DEX via activation of Keap1-Nrf2 signaling cascade.

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Section: Methodsmentioning

confidence: 99%

PGK1 depletion activates Nrf2 signaling to protect human osteoblasts from dexamethasone

et al. 2019

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“…As reported 13,16 , NSCLC cells (in serum free medium, 4 × 10,000 cells per chamber) were seeded at the upper surfaces of "Transwell" chambers (BD Biosciences, Heidelberg, Germany). The lower compartments were filled with FBS-containing complete medium.…”

Section: Cell Migration and Invasion Assaysmentioning

confidence: 99%

“…As described 13,16,17 , an equal amount protein lysates (30-40 μg per treatment in each lane) were separated by 10-12% SDSPAGE gels and thereafter transferred onto PVDF blots. Membranes were blocked and incubated with indicated primary antibodies, and subsequently incubated with corresponding secondary antibodies.…”

Section: Western Blottingmentioning

confidence: 99%

GDC-0349 inhibits non-small cell lung cancer cell growth

Han

Zhao

et al. 2020

Cell Death Dis

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Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related human mortality with a clear need for new therapeutic intervention. GDC-0349 is a potent and selective ATP-competitive mTOR inhibitor. In A549 cells and primary human NSCLC cells, GDC-0349 inhibited cell growth, proliferation, cell cycle progression, migration and invasion, while inducing significant apoptosis activation. Although GDC-0349 blocked Akt-mTORC1/2 activation in NSCLC cells, it also exerted cytotoxicity in Akt1-knockout A549 cells. Furthermore, restoring Akt-mTOR activation by a constitutively-active Akt1 only partially attenuated GDC-0349-induced A549 cell apoptosis, indicating the existence of Akt-mTOR-independent mechanisms. In NSCLC cells GDC-0349 induced sphingosine kinase 1 (SphK1) inhibition, ceramide accumulation, JNK activation and oxidative injury. Conversely, N-acetylcysteine, the JNK inhibitor and sphingosine 1-phosphate alleviated GDC-0349-induced NSCLC cell apoptosis. In vivo, daily oral administration of GDC-0349 potently inhibited NSCLC xenograft growth in mice. Akt-mTOR in-activation, SphK1 inhibition, JNK activation and oxidative stress were detected in NSCLC xenograft tissues with GDC-0349 administration. In summary, GDC-0349 inhibits NSCLC cell growth via Akt-mTOR-dependent and Akt-mTOR-independent mechanisms.

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“…In hepatocellular carcinoma, circTRIM33-12 has thus far been verified to induce tumorigenesis via its action as a buffering molecule for miR-191 [13]. Specifically, in lung cancer circRNA circPRKCI stimulates tumor cell growth through a ceRNA mechanism [14]. In pancreatic cancer, circ-LDLRAD3 was found to be significantly associated with lymphatic/venous invasion and metastasis [15].…”

Section: Introductionmentioning

confidence: 99%

CircRNA_0058063 functions as a ceRNA in bladder cancer progression via targeting miR-486-3p/FOXP4 axis

Liang

Huang

et al. 2020

Bioscience Reports

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Emerging evidence has uncovered critical regulatory roles of circular RNAs (circRNAs) function as dynamic scaffolding molecules in tumorigenesis and progression. However, the aberrant expression and clinical significance of hsa_circ_0058063 (circRNA_0058063) in bladder cancer (BC) remain poorly understood. circRNA expression was analyzed via a microarray in cancerous tissue and non-carcinoma tissues. Luciferase reporter assays and RNA immunoprecipitation (RIP) were both conducted to uncover the function of circRNA_0058063 in BC. circRNA_0058063 was overexpressed in BC tissues compared with adjacent normal tissues. Knockdown of circRNA_0058063 dramatically decreased cell proliferation and invasion, and promoted apoptosis in 5637 and BIU-87 cell lines. Furthermore, mechanistic investigations showed that circRNA_0058063 and FOXP4 could directly bind to miR-486-3p, demonstrating that circRNA_0058063 regulated FOXP4 expression by competitively binding to miR-486-3p. Taken together, circRNA_0058063 functions by sponging miR-486-3p in BC progression, which could act as a new biomarker and further developed to be a therapeutic target in BC.

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Circular RNA PRKCI promotes glioma cell progression by inhibiting microRNA-545

Cited by 31 publications

References 40 publications

PGK1 depletion activates Nrf2 signaling to protect human osteoblasts from dexamethasone

PGK1 depletion activates Nrf2 signaling to protect human osteoblasts from dexamethasone

GDC-0349 inhibits non-small cell lung cancer cell growth

CircRNA_0058063 functions as a ceRNA in bladder cancer progression via targeting miR-486-3p/FOXP4 axis

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