Long noncoding RNA IGF2AS regulates high‐glucose induced apoptosis in human retinal pigment epithelial cells

Yu, Xiaoyi; Luo, Yi; Chen, Gangyi; Liu, Hong; Tian, Ni; Zen, Xiaoting; Liu, Qiuhong

doi:10.1002/iub.2102

Cited by 18 publications

(14 citation statements)

References 28 publications

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“…Previous studies have highlighted the importance of HDAC6 inhibition in regulating oxidative stress and inflammation in a variety of diseases, especially in DR (Shi et al 2017;Yi et al 2019;Zhang et al 2019a). The effect of Cay, a novel inhibitor of HDAC6, was investigated in this research, and we demonstrated that Cay treatment It is also worth noting that robust evidence suggests that sustained hyperglycemia triggers apoptosis in RPE cells, which is a major pathological change in the eyes of patients with DR (Willermain et al 2018;Yu et al 2019;Zhang et al 2019b). Numerous studies unveil that inhibition of apoptosis of RPE cells contributes to protect against DR (Jiang et al 2017;Yu et al 2018).…”

Section: Discussionmentioning

confidence: 66%

HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-κB and NLRP3 inflammasome pathway

Yang

Li²,

Zhou³

et al. 2020

gpb

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The present study aimed to investigate the effects of histone deacetylase 6 (HDAC6) inhibitor Cay10603 (Cay) on high glucose (HG)-stimulated human retinal pigment epithelium (RPE) cells and its underlying mechanisms. ARPE-19 cells were cultured under normal glucose (NG) or high glucose (HG) conditions. The results revealed that HDAC6 was upregulated in HG-stimulated ARPE-19 cells. Cay treatment caused a decrease in intracellular reactive oxygen species (ROS). The levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were reduced accompanied by increase in the activities of superoxide dismutase (SOD) and catalase (CAT) after treatment with Cay. Besides, Cay decreased the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and monocyte chemoattractant protein-1 (MCP-1) in supernatant. Meanwhile, the apoptotic rate in Cay-treated ARPE-19 cells notably reduced, coupled with an upregulation in Bcl-2 expression and a downregulation in cleaved caspase-3 and cleaved caspase-9 expression. Cay decreased the expression of phospho (p)-NF-κB p65, p-IκB-α, NLRP3, cleaved caspase-1 and ASC while increased the expression of NF-κB p65 (cytoplasm). Taken together, these findings demonstrated that Cay suppressed HG-induced oxidative stress, inflammation and apoptosis via regulating NF-κB and NLRP3 inflammasome pathway in HG-induced ARPE-19 cells, suggesting that Cay might be a therapeutic agent for the treatment of diabetic retinopathy.

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Section: Discussionmentioning

confidence: 66%

HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-κB and NLRP3 inflammasome pathway

Yang

Li²,

Zhou³

et al. 2020

gpb

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“…However, to date, no protein has yet been identified. There have, however, been a number of reports that IGF-IIas may function epigenetically as a lncRNA with effects on cell proliferation and invasion [61], apoptosis [62], and angiogenesis [63]. All of these reports found that these effects of IGF-IIas were reversed by increased expression of IGF-II and were consistent with an effect of IGF-IIas to suppress IGF-II expression even though no actual mechanism for this has yet been confirmed.…”

Section: Igf-ii: An Imprinted Multifunctional Metabolic Genetic Locimentioning

confidence: 99%

The Neglected Insulin: IGF-II, a Metabolic Regulator with Implications for Diabetes, Obesity, and Cancer

Holly

Biernacka

Perks

2019

Cells

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When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a result of gene duplication, but has evolved to be considerably more complicated. It was one of the first genes recognised to be imprinted and expressed in a parent-of-origin specific manner. The gene codes for IGF-II mRNA, but, in addition, also codes for antisense RNA, long non-coding RNA, and several micro RNA. Recent evidence suggests that each of these have important independent roles in metabolic regulation. It has also become clear that an alternatively spliced form of the insulin receptor may be the principle IGF-II receptor. These recent discoveries have important implications for metabolic disorders and also for cancer, for which there is renewed acknowledgement of the importance of metabolic reprogramming.

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“…6 Recently, a novel lncRNA, IGF2 antisense RNA (IGF2-AS), was identified as a critical player in human disease. IGF2-AS was proposed to be closely associated with high-glucose-induced apoptosis in diabetic retinopathy 7 and angiogenesis in type 2 diabetes. 8 Moreover, IGF2-AS was shown to be activated by STAT3, and increased hepatitis C virus replication.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA IGF2-AS represses breast cancer tumorigenesis by epigenetically regulating IGF2

Zhang¹,

Yan

Jiang

et al. 2020

Exp Biol Med (Maywood)

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Long non-coding RNAs are a kind of endogenous ncRNAs with a length of more than 200 bp. Accumulating evidence suggests that long non-coding RNAs function as pivotal regulators in tumorigenesis and progression. However, their biological roles in breast cancer remain largely unknown. Here, we found that IGF2 antisense RNA (IGF2-AS) was significantly decreased in breast cancer tissues, cell lines, and plasma. Patients with low IGF2-AS were more likely to develop larger tumor size and later clinical stage. Overexpression of IGF2-AS evidently inhibited the proliferation and induced apoptosis of MCF-7 and T47D cells in vitro, as well as retarded tumor growth in vivo. Further investigation revealed that IGF2-AS inhibited the expression of its sense-cognate gene IGF2 in an epigenetic DNMT1-dependent manner, resulting in the inactivation of downstream oncogenic PI3K/AKT/mTOR signaling pathway. Enforced expression of IGF2 could significantly block the tumor inhibitory effect of IGF2-AS. Importantly, we found that IGF2-AS could be used as an effective biomarker for breast cancer diagnosis and prognosis. Taken together, our study indicates that IGF2-AS is a tumor suppressor in breast cancer, restoration of IGF2-AS may be a promising treatment for this fatal disease.

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Long noncoding RNA IGF2AS regulates high‐glucose induced apoptosis in human retinal pigment epithelial cells

Cited by 18 publications

References 28 publications

HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-κB and NLRP3 inflammasome pathway

HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-κB and NLRP3 inflammasome pathway

The Neglected Insulin: IGF-II, a Metabolic Regulator with Implications for Diabetes, Obesity, and Cancer

Long non-coding RNA IGF2-AS represses breast cancer tumorigenesis by epigenetically regulating IGF2

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