lncRNA PINK1-AS Aggravates Cerebral Ischemia/Reperfusion Oxidative Stress Injury through Regulating ATF2 by Sponging miR-203

Yang, Zhong‐Bao; Yu, Xiang; Zuo, Mei-Lin; Li, Mao; Hu, Guo‐Huang; Song, Gui-Lin; Sheikh, Sayed Ali; Tan, Liming

doi:10.1155/2022/1296816

Cited by 7 publications

(8 citation statements)

References 30 publications

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“…PINK1-AS knockdown increases ROS levels in glioma cells, promotes mitochondrial ssion, and decreases aerobic glucose metabolism levels in glioma. However, one study reported a positive correlation between PINK1-AS expression level and ROS production level [17]. This may be affected by differences in cell lines or stages of disease development.…”

Section: Discussionmentioning

confidence: 98%

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Parkinson’s disease-related lncRNA PINK1-AS advances glioma oncogenesis by regulating the YAP1-Hippo signaling pathway

Sun

Wang

et al. 2023

Preprint

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Background Epidemiological studies have demonstrated a higher incidence of gliomas in patients with Parkinson’s disease (PD). However, the underlying molecular mechanisms remain unclear, and insights into why and how patients with PD are susceptible to glioma are essential for advancing novel therapeutic approaches for both diseases. Therefore, we investigate the function of PD-related lncRNA PINK1-AS in glioma progression.Methods The expression of the long non-coding PTEN-induced kinase 1 antisense RNA gene (PINK1-AS) in PD and glioma tissues and cells was characterized by quantitative reverse transcription polymerase chain reaction. The efficacy of PINK1-AS knockdown in glioma cell lines was evaluated by assessing cell proliferation, migration, and cell cycles. In addition, experimental xenografts were administered to nude mice to evaluate the effect of PINK1-AS on gliomas. To establish the relationship between the PINK1-AS, miR-200a, and yes-associated protein 1 (YAP1) genes, RNA immunoprecipitation, RNA probe pull-down, luciferase reporter, and fluorescence in situ hybridization assays were performed.Results PINK1-AS expression was anomalously elevated in PD, glioma tissues, and cell lines compared to normal brain tissue, and the overall survival time was reduced in patients with glioma with high PINK1-AS expression. PINK1-AS knockdown remarkably suppressed glioma metaplasia, including cell promotion, metastasis, and aggression in vitro and xenograft tumor generation in vivo. Furthermore, PINK1-AS targeted miR-200a, and miR-200a inhibition inverted the virulent features of PINK1-AS knockdown on glioma cells. Specifically, PINK1-AS may serve as a competing endogenous RNA that effectively functions as a pool for miR-200a, thereby de-repressing YAP1.Conclusions PINK1-AS is a key inhibitor of the Hippo signaling pathway by inhibiting miR-200a, and targeting PINK1-AS may be a novel therapeutic strategy for patients with glioma, especially those with PD.

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Section: Discussionmentioning

confidence: 98%

“…Thus, PINK1-AS is closely associated with PD development and occurrence. Additionally, PINK1-AS is associated with gastric cancer tumorigenesis and cerebral ischemia/reperfusion oxidative stress injury [16,17]; however, its role in glioma remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Parkinson’s disease-related lncRNA PINK1-AS advances glioma oncogenesis by regulating the YAP1-Hippo signaling pathway

Sun

Wang

et al. 2023

Preprint

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“…In endothelial cells, for example, a correlation between Mir7 and Pink1 seems to exist [55]. A causal relationship between the Mir203 and Pink1 was also shown for neurons [55,56]. To what extent these are cell line-specific effects and whether these mechanisms are relevant to tumor cells must currently remain open.…”

Section: Genes Related To Tumor Progressionmentioning

confidence: 99%

The Role of microRNAs in Gene Expression and Signaling Response of Tumor Cells to an Acidic Environment

Riemann,

Rauschner,

Reime

et al. 2023

IJMS

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Many tumors are characterized by marked extracellular acidosis due to increased glycolytic metabolism, which affects gene expression and thereby tumor biological behavior. At the same time, acidosis leads to altered expression of several microRNAs (Mir7, Mir183, Mir203, Mir215). The aim of this study was to analyze whether the acidosis-induced changes in cytokines and tumor-related genes are mediated via pH-sensitive microRNAs. Therefore, the expression of Il6, Nos2, Ccl2, Spp1, Tnf, Acat2, Aox1, Crem, Gls2, Per3, Pink1, Txnip, and Ypel3 was examined in acidosis upon simultaneous transfection with microRNA mimics or antagomirs in two tumor lines in vitro and in vivo. In addition, it was investigated whether microRNA expression in acidosis is affected via known pH-sensitive signaling pathways (MAPK, PKC, PI3K), via ROS, or via altered intracellular Ca2+ concentration. pH-dependent microRNAs were shown to play only a minor role in modulating gene expression. Individual genes (e.g., Ccl2, Txnip, Ypel3) appear to be affected by Mir183, Mir203, or Mir215 in acidosis, but these effects are cell line-specific. When examining whether acid-dependent signaling affects microRNA expression, it was found that Mir203 was modulated by MAPK and ROS, Mir7 was affected by PKC, and Mir215 was dependent on the intracellular Ca2+ concentration. Mir183 could be increased by ROS scavenging. These correlations could possibly result in new therapeutic approaches for acidotic tumors.

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“…It has been found that NADPH oxidase 2 (NOX2) plays a key role in CI/R-induced oxidative stress injury and is a key enzyme causing ROS [ 63 ]. In addition, several studies showed that decreasing NOX2 expression and reducing NOX activity are two effective ways to attenuate CIRI [ 64 ]. When studying the protective mechanism of ischemic preconditioning, some researchers found that ischemic preconditioning (IPC) can induce cerebral ischemic tolerance, which is initiated by oxidative stress.…”

Section: Oxidative Stress and Cerebral Ischemic Strokementioning

confidence: 99%

Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke

et al. 2022

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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.

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lncRNA PINK1-AS Aggravates Cerebral Ischemia/Reperfusion Oxidative Stress Injury through Regulating ATF2 by Sponging miR-203

Cited by 7 publications

References 30 publications

Parkinson’s disease-related lncRNA PINK1-AS advances glioma oncogenesis by regulating the YAP1-Hippo signaling pathway

Parkinson’s disease-related lncRNA PINK1-AS advances glioma oncogenesis by regulating the YAP1-Hippo signaling pathway

The Role of microRNAs in Gene Expression and Signaling Response of Tumor Cells to an Acidic Environment

Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke

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