Role of <scp>TGF</scp>‐β1/miR‐382‐5p/<scp>SOD</scp>2 axis in the induction of oxidative stress in <scp>CD</scp>34+ cells from primary myelofibrosis

Rossi, Chiara; Zini, Roberta; Rontauroli, Sebastiano; Ruberti, Samantha; Prudente, Zelia; Barbieri, Greta; Bianchi, Elisa; Salati, Simona; Genovese, Elena; Bartalucci, Niccolò; Guglielmelli, Paola; Tagliafico, Enrico; Rosti, Vittorio; Barosi, Giovanni; Vannucchi, Alessandro M.; Manfredini, Rossella

doi:10.1002/1878-0261.12387

Cited by 20 publications

(10 citation statements)

References 54 publications

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“…It was reported that miR-382-5p may engaged in various cancers. For instance, there was an upregulation of miR-382-5p in primary myelofibrosis cells [7], but the expression of miR-382-5p was downregulated in glioma-exposed endothelial cells [8]. But there have been no studies about circRNA-UBAP2 regulated miR-382-5p.…”

Section: Introductionmentioning

confidence: 99%

circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis

Deng

et al. 2020

J Ovarian Res

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Objective: circular RNAs (circRNAs) have been reported to be essential regulators of multiple malignant cancers. However, the functions of circRNAs in ovarian cancer need to be further explored. The aim of our study is to explore the role of circRNA-UBAP2 in ovarian cancer and its mechanism. Results: circRNA-UBAP2 was upregulated in ovarian cancer tissues and cell lines. Knockdown of circRNA-UBAP2 inhibited cell proliferation and promoted cell apoptosis, but circRNA-UBAP2 overexpressed got opposite results. In addition, circRNA-UBAP2 targeted miR-382-5p and downregulated its expression, PRPF8 was a target gene of miR-382-5p. Furthemore, circRNA-UBAP2/miR-382-5p/PRPF8 axis affected the proliferation, apoptosis and cell cycle of ovarian cancer through the mechanism of competing endogenous RNAs (ceRNA). Conclusion: circRNA-UBAP2 acted as a ceRNA to sponged miR-382-5p, increased the expression level of PRPF8, and prompted proliferation and inhibited apoptosis in ovarian cancer cells.

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Section: Introductionmentioning

confidence: 99%

circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis

Deng

et al. 2020

J Ovarian Res

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“…The TGF-β superfamily, including activins, growth differentiation factors and bone morphogenetic proteins, plays a major role during signaling in the BM niche, being able to promote oxidative stress, myeloproliferation and fibrosis [ 55 , 85 , 158 ]. Sotatercept and luspatercept are erythroid maturation agents that work as activin receptor ligand traps of IIA and IIB, respectively [ 159 , 160 , 161 , 162 ].…”

Section: Looking For the Achilles’ Heel In Mpns: Innovative Targetmentioning

confidence: 99%

Inflammatory Microenvironment and Specific T Cells in Myeloproliferative Neoplasms: Immunopathogenesis and Novel Immunotherapies

Nasillo

Riva

Paolini

et al. 2021

IJMS

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The Philadelphia-negative myeloproliferative neoplasms (MPNs) are malignancies of the hematopoietic stem cell (HSC) arising as a consequence of clonal proliferation driven by somatically acquired driver mutations in discrete genes (JAK2, CALR, MPL). In recent years, along with the advances in molecular characterization, the role of immune dysregulation has been achieving increasing relevance in the pathogenesis and evolution of MPNs. In particular, a growing number of studies have shown that MPNs are often associated with detrimental cytokine milieu, expansion of the monocyte/macrophage compartment and myeloid-derived suppressor cells, as well as altered functions of T cells, dendritic cells and NK cells. Moreover, akin to solid tumors and other hematological malignancies, MPNs are able to evade T cell immune surveillance by engaging the PD-1/PD-L1 axis, whose pharmacological blockade with checkpoint inhibitors can successfully restore effective antitumor responses. A further interesting cue is provided by the recent discovery of the high immunogenic potential of JAK2V617F and CALR exon 9 mutations, that could be harnessed as intriguing targets for innovative adoptive immunotherapies. This review focuses on the recent insights in the immunological dysfunctions contributing to the pathogenesis of MPNs and outlines the potential impact of related immunotherapeutic approaches.

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“…MnSOD (SOD2) is targeted by several miRNAs including miR-17-3p, miR-23a, miR-146a, miR-212, miR-222, miR-335, miR-382-5p, and miR-575 [98][99][100][101][102][103][104][105][106]. In prostate cancer cells miR-17-3p targets MnSOD, GPX2, and TXNRD2 leading to ROS accumulation [98].…”

Section: Regulation Of Superoxide Dismutases By Mirnasmentioning

confidence: 99%

Micro RNAs in Regulation of Cellular Redox Homeostasis

Ciesielska

Ślęzak-Prochazka

Bil

et al. 2021

IJMS

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In living cells Reactive Oxygen Species (ROS) participate in intra- and inter-cellular signaling and all cells contain specific systems that guard redox homeostasis. These systems contain both enzymes which may produce ROS such as NADPH-dependent and other oxidases or nitric oxide synthases, and ROS-neutralizing enzymes such as catalase, peroxiredoxins, thioredoxins, thioredoxin reductases, glutathione reductases, and many others. Most of the genes coding for these enzymes contain sequences targeted by micro RNAs (miRNAs), which are components of RNA-induced silencing complexes and play important roles in inhibiting translation of their targeted messenger RNAs (mRNAs). In this review we describe miRNAs that directly target and can influence enzymes responsible for scavenging of ROS and their possible role in cellular redox homeostasis. Regulation of antioxidant enzymes aims to adjust cells to survive in unstable oxidative environments; however, sometimes seemingly paradoxical phenomena appear where oxidative stress induces an increase in the levels of miRNAs which target genes which are supposed to neutralize ROS and therefore would be expected to decrease antioxidant levels. Here we show examples of such cellular behaviors and discuss the possible roles of miRNAs in redox regulatory circuits and further cell responses to stress.

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Role of TGF‐β1/miR‐382‐5p/SOD2 axis in the induction of oxidative stress in CD34+ cells from primary myelofibrosis

Cited by 20 publications

References 54 publications

circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis

circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis

Inflammatory Microenvironment and Specific T Cells in Myeloproliferative Neoplasms: Immunopathogenesis and Novel Immunotherapies

Micro RNAs in Regulation of Cellular Redox Homeostasis

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