miR-491-5p regulates the susceptibility of glioblastoma to ferroptosis through TP53

Jie, Xinfang; Liu, Yunpeng; Liu, Shuai; Fu, Yubin; Xiong, Yuanyuan

doi:10.1016/j.bbrc.2023.05.057

Cited by 3 publications

(3 citation statements)

References 39 publications

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“…41,42 In addition, miR-491-5p exerts Several target genes of miR-491-5p, including emilin 1, TP53 and metallothionein-2, could be dramatically repressed by miR-491-5p via binding to 3' UTRs. 24,27,41 USP13 is a deubiquitinase that modulates cancer progression, immune inflammatory response, metabolism disorder. 28 Several studies have shown that USP13 exerted important functions in modulating lung fibrosis and ECM deposition.…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNA-491-5p (miR-491-5p) acts as a tumor suppressor in several cancers, such as glioblastoma, hepatocellular carcinoma and pancreatic cancer, and can modulate ferroptosis and fibrosis of contraction bands fibroblasts. [24][25][26] miR-491-5p expression was reduced in Hep3B cells, and miR-491-5p overexpression could repress Hep3B cells proliferation, migration and invasion. 25 In addition, miR-491-5p overexpression facilitated fibroblasts growth and fibrosis of contraction bands fibroblasts, as well as elevated α-SMA, Collagen I, and Collagen III expression.…”

mentioning

confidence: 94%

“…27 Moreover, miR-491-5p overexpression repressed ferroptosis by reducing ROS level and iron ion level in glioblastoma. 24 However, whether miR-491-5p modulates ferroptosis and ECM deposition of activated HSCs in liver fibrosis is not discovered.…”

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confidence: 99%

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LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

Li,

Zou,

Jin

et al. 2024

Environmental Toxicology

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Liver fibrosis is an invertible pathophysiologic process featured by excessive accumulation of extracellular matrix (ECM) which injures liver cells and activates hepatic stellate cells (HSCs). Besides, inducing ferroptosis in activated HSCs can alleviate liver fibrosis. LncRNAs modulate ferroptosis in activated HSCs and ECM deposition in liver fibrosis. However, the role of lncRNA FRMD6‐AS1 in liver fibrosis is not discovered. In this study, lncRNA FRMD6‐AS1 was dramatically up‐regulated in activated HSCs. Knockdown of FRMD6‐AS1 markedly increased iron ion, ROS and MDA levels, decreased GSH level, SLC7A11 and GPX4 protein expressions in activated HSCs. In addition, HSCs activation markers α‐SMA and COL1α1 expressions were up‐regulated in activated HSCs; knockdown of FRMD6‐AS1 markedly down‐regulated α‐SMA and COL1α1 expressions in HSCs. Besides, lncRNA FRMD6‐AS1 could interact with miR‐491‐5p, and negatively modulate miR‐491‐5p expression. USP13 was a target of miR‐491‐5p, and could be negatively modulated by miR‐491‐5p. Moreover, FRMD6‐AS1 knockdown increased iron ion and ROS levels, decreased SLC7A11 and GPX4 protein expressions, facilitated HSCs viability, and up‐regulated α‐SMA and COL1α1 expressions via miR‐491‐5p/USP13 pathway. Finally, FRMD6‐AS1 knockdown restored liver tissue structure and abrogated fibrosis in livers in a CCL4 liver fibrosis mouse model. Hence, lncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway repressed ferroptosis, promoted ECM deposition and facilitated liver fibrosis in vitro and in vivo models.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 94%

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LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

Li,

Zou,

Jin

et al. 2024

Environmental Toxicology

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Disrupted glutamate homeostasis as a target for glioma therapy

Biegański,

Szeliga

2024

Pharmacol. Rep

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Glutamate is the major excitatory neurotransmitter in the central nervous system (CNS). Gliomas, malignant brain tumors with a dismal prognosis, alter glutamate homeostasis in the brain, which is advantageous for their growth, survival, and invasion. Alterations in glutamate homeostasis result from its excessive production and release to the extracellular space. High glutamate concentration in the tumor microenvironment destroys healthy tissue surrounding the tumor, thus providing space for glioma cells to expand. Moreover, it confers neuron hyperexcitability, leading to epilepsy, a common symptom in glioma patients. This mini-review briefly describes the biochemistry of glutamate production and transport in gliomas as well as the activation of glutamate receptors. It also summarizes the current pre-clinical and clinical studies identifying pharmacotherapeutics targeting glutamate transporters and receptors emerging as potential therapeutic strategies for glioma.

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ActivinA modulates B-acute lymphoblastic leukaemia cell communication and survival by inducing extracellular vesicles production

Licari,

Cricrì,

Mauri

et al. 2024

Sci Rep

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Extracellular vesicles (EVs) are a new mechanism of cellular communication, by delivering their cargo into target cells to modulate molecular pathways. EV-mediated crosstalk contributes to tumor survival and resistance to cellular stress. However, the role of EVs in B-cell Acute Lymphoblastic Leukaemia (B-ALL) awaits to be thoroughly investigated. We recently published that ActivinA increases intracellular calcium levels and promotes actin polymerization in B-ALL cells. These biological processes guide cytoskeleton reorganization, which is a crucial event for EV secretion and internalization. Hence, we investigated the role of EVs in the context of B-ALL and the impact of ActivinA on this phenomenon. We demonstrated that leukemic cells release a higher number of EVs in response to ActivinA treatment, and they can actively uptake EVs released by other B-ALL cells. Under culture-induced stress conditions, EVs coculture promoted cell survival in B-ALL cells in a dose-dependent manner. Direct stimulation of B-ALL cells with ActivinA or with EVs isolated from ActivinA-stimulated cells was even more effective in preventing cell death. This effect can be possibly ascribed to the increase of vesiculation and modifications of EV-associated microRNAs induced by ActivinA. These data demonstrate that ActivinA boosts EV-mediated B-ALL crosstalk, improving leukemia survival in stress conditions.

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miR-491-5p regulates the susceptibility of glioblastoma to ferroptosis through TP53

Cited by 3 publications

References 39 publications

LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

Disrupted glutamate homeostasis as a target for glioma therapy

ActivinA modulates B-acute lymphoblastic leukaemia cell communication and survival by inducing extracellular vesicles production

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