ArticleEnvironmental geochemistry and health2021
Inorganic arsenic influences cell apoptosis by regulating the expression of MEG3 gene.
Article in Environmental geochemistry and health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Long Non-Coding RNA MEG3 in Metal Carcinogenesis.Toxics · 2023Review
- The multifaceted biology of lncR-Meg3 in cardio-cerebrovascular diseases.Frontiers in genetics · 2023Review
- Toxicoepigenetics and Environmental Health: Challenges and Opportunities.Chemical research in toxicology · 2022Review
- Associations and Interactions between Heavy Metals with White Blood Cell and Eosinophil Count.International journal of medical sciences · 2022Article
- Phloretin Alleviates Arsenic Trioxide-Induced Apoptosis of H9c2 Cardiomyoblasts via Downregulation in CaCardiovascular toxicology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Arsenic is a wildly distributed carcinogen in the environment. Arsenic-induced apoptosis has been extensively studied in therapeutics and toxicology. LncRNA MEG3 has been extensively studied as apoptosis regulatory gene in recent years. However, it stays unclear regarding how the mechanism of MEG3 regulates arsenic-induced apoptosis. Our focus was to explore the effects of MEG3 on arsenic-induced apoptosis. MTS assay was used to test cell viability, and qRT-PCR was for the examination of gene expressions. The effect of the apoptosis and necrosis after knockdown MEG3 was detected with double staining. Our results demonstrated that MEG3 expression was positively correlated with the concentration of three arsenic species (inorganic arsenic (iAs), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA)) (p < 0.05). The ability of iAs to induce MEG3 expression was much higher compared with that induced by MMA and DMA. In addition, our experiments confirmed that MEG3 knockdown increased cell viability and arsenic-induced apoptosis, but cell viability decreased after iAs treatment. Moreover, LncRNA MEG3 regulated apoptosis via down-regulate API5 while up-regulate CASP7, CCND3 and APAF1. It is further proved that arsenic-induced apoptosis increased after the knockdown of MEG3, which regulates these genes. These findings provide experimental evidence and possible mechanisms for subsequent research on the effects of arsenic on health.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.