MicroRNA-670-3p suppresses ferroptosis of human glioblastoma cells through targeting ACSL4

Bao, Chong; Zhang, Jing; Xian, Shu-Yue; Chen, Feng

doi:10.1080/10715762.2021.1962009

Cited by 41 publications

(41 citation statements)

References 68 publications

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“…To investigate whether the miR-147a inhibitor could prevent ferroptosis, cells were transfected with the miR-147a inhibitor (50 nmol/L) for 4 h and then stimulated with erastin (5 μ mol/L) or RSL3 (2 μ mol/L) for an additional 72 h. To overexpress SLC40A1, cells were infected with AdSLC40A1 at a multiplicity of infection of 20 for 4 h and maintained in fresh DMEM containing 10% FBS for an additional 24 h before the miR-147a mimic transfection. In a separated study, cells with or without the miR-147a mimic transfection were treated with TMZ (100 μ mol/L) for 48 h to determine whether overexpressing miR-147a could sensitize glioblastoma cells to TMZ chemotherapy [ 28 ].…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-147a Targets SLC40A1 to Induce Ferroptosis in Human Glioblastoma

et al. 2022

Analytical Cellular Pathology

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Objective. Glioblastoma is one of the most common malignant tumors in the brain, and these glioblastoma patients have very poor prognosis. Ferroptosis is involved in the progression of various tumors, including the glioblastoma. This study aims to determine the involvement of microRNA (miR)-147a in regulating ferroptosis of glioblastoma in vitro. Methods. Human glioblastoma cell lines were transfected with the inhibitor, mimic and matched negative controls of miR-147a in the presence or absence of ferroptotic inducers. To knock down the endogenous solute carrier family 40 member 1 (SLC40A1), cells were transfected with the small interfering RNA against SLC40A1. In addition, cells with or without the miR-147a mimic treatment were also incubated with temozolomide (TMZ) to investigate whether miR-147a overexpression could sensitize human glioblastoma cells to TMZ chemotherapy in vitro. Results. We found that miR-147a level was decreased in human glioblastoma tissues and cell lines and that the miR-147a mimic significantly suppressed the growth of glioblastoma cells in vitro. In addition, miR-147a expression was elevated in human glioblastoma cells upon erastin or RSL3 stimulation. Treatment with the miR-147a mimic significantly induced ferroptosis of glioblastoma cells, and the ferroptotic inhibitors could block the miR-147a mimic-mediated tumor suppression in vitro. Conversely, the miR-147a inhibitor prevented erastin- or RSL3-induced ferroptosis and increased the viability of glioblastoma cells in vitro. Mechanistically, we determined that miR-147a directly bound to the 3 ′ -untranslated region of SLC40A1 and inhibited SLC40A1-mediated iron export, thereby facilitating iron overload, lipid peroxidation, and ferroptosis. Furthermore, miR-147a mimic-treated human glioblastoma cells exhibited higher sensitivity to TMZ chemotherapy than those treated with the mimic control in vitro. Conclusion. We for the first time determine that miR-147a targets SLC40A1 to induce ferroptosis in human glioblastoma in vitro.

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Section: Methodsmentioning

confidence: 99%

MicroRNA-147a Targets SLC40A1 to Induce Ferroptosis in Human Glioblastoma

et al. 2022

Analytical Cellular Pathology

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“…159 MiR-670-3p can then inhibit human glioblastoma ferroptosis by downregulating ACSL4 expression. 160 Additionally, GPX4 and FSP1, key peroxidation inhibitors of ferroptosis, are highly expressed in gliomas, inhibiting cellular ferroptosis and promoting glioma survival. 161 Targeting and regulating key proteins of ferroptosis to induce ferroptosis would potentially inhibit glioma cell proliferation.…”

Section: Gliomamentioning

confidence: 99%

Ferroptosis and Its Potential Role in the Nervous System Diseases

Zhou¹,

Lin²,

Rao³

et al. 2022

JIR

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Ferroptosis is a novel regulated cell death characterized by metabolic disorders and iron-dependent oxidative destruction of the lipid bilayer. It is primarily caused by the imbalance of oxidation and anti-oxidation in the body and is precisely regulated by numerous factors and pathways inside and outside the cell. Recent studies have indicated that ferroptosis plays a vital role in the pathophysiological process of multiple systems of the body including the nervous system. Ferroptosis may be closely linked to the occurrence and development of neurodegenerative diseases, strokes, and brain tumors. It may also be involved in the development, maturation, and aging of the nervous system. Therefore, this study aims to investigate ferroptosis's occurrence and regulatory mechanism and summarize its research progress in the pathogenesis and treatment of neurological diseases. This would allow for novel ideas for basic and clinical research of neurological diseases.

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“…Thus, ferroptosis has a pro-tumorigenic role in early tumour progression by participating in the necrosis process, further enhancing the process by neutrophils recruitment that further increase ferroptosis and necrosis [117]. Suppressing the ACSL4 pathway reduces tumour progression and, furthermore, it increases the tumour sensibility to TMZ treatment [118].…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Ferroptosis Involvement in Glioblastoma Treatment

et al. 2022

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Glioblastoma multiforme (GBM) is one of the deadliest brain tumors. Current standard therapy includes tumor resection surgery followed by radiotherapy and chemotherapy. Due to the tumors invasive nature, recurrences are almost a certainty, giving the patients after diagnosis only a 12–15 months average survival time. Therefore, there is a dire need of finding new therapies that could potentially improve patient outcomes. Ferroptosis is a newly described form of cell death with several implications in cancer, among which GBM. Agents that target different molecules involved in ferroptosis and that stimulate this process have been described as potentially adjuvant anti-cancer treatment options. In GBM, ferroptosis stimulation inhibits tumor growth, improves patient survival, and increases the efficacy of radiation and chemotherapy. This review provides an overview of the current knowledge regarding ferroptosis modulation in GBM.

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MicroRNA-670-3p suppresses ferroptosis of human glioblastoma cells through targeting ACSL4

Cited by 41 publications

References 68 publications

MicroRNA-147a Targets SLC40A1 to Induce Ferroptosis in Human Glioblastoma

MicroRNA-147a Targets SLC40A1 to Induce Ferroptosis in Human Glioblastoma

Ferroptosis and Its Potential Role in the Nervous System Diseases

Ferroptosis Involvement in Glioblastoma Treatment

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