Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 556, Issue -, Pages 72-78Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.03.132
Keywords
Long non-coding RNA MEG8; miR-497-5p; NOTCH2; Hemangioma; Ferroptosis
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Funding
- National Key Research and Development Project [2017YFB0403801, 2018YFB0407201]
- Joint Special Program of Yunnan Province Department and Kunming Medical University [2019FE001(-111)]
- Application base project of Yunnan Science and Technology Department [2019FB097]
- Yunnan health training project of high level talents [D-2018005]
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The study revealed that long non-coding RNA MEG8 inhibits the proliferation of hemangioma endothelial cells by regulating the miR-497-5p/NOTCH2 axis and induces ferroptosis.
Even though long non-coding RNA (lncRNA) MEG8 plays vital roles in carcinogenesis of malignances, its roles and mechanisms in hemangioma remain unknown. Therefore, we evaluate the oncogenic roles of MEG8 in hemangioma. Small interfering RNA (siRNA)-mediated depletion of MEG8 inhibited the proliferation and increased MDA level in human hemangioma endothelial cells (HemECs). The inhibitors of ferroptosis (ferrostatin-1 and liproxstatin-1) abolished the MEG8 silence induced cell viability loss. Knockdown of MEG8 increased the miR-497-5p expression and reduced the mRNA and protein levels of NOTCH2. Using a dual-luciferase assay, we confirmed the binding between MEG8 and miR-497-5p, and between the miR-497-5p and 3'UTR of NOTCH2. We further found that silencing MEG8 significantly decreased the expressions of SLC7A11 and GPX4 both in mRNA and protein level and had no effect on the level of AIFM2. Importantly, blocking miR-497-5p abrogated the effects of MEG8 loss on cell viability, MDA level and expression levels of NOTCH2, SLC7A11 and GPX4 in HemECs. Taken together, our results suggested that knockdown of long non-coding RNA MEG8 inhibited the proliferation and induced the ferroptosis of hemangioma endothelial cells by regulating miR-497-5p/NOTCH2 axis. (C) 2021 Elsevier Inc. All rights reserved.
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