BACH1, the master regulator gene: A novel candidate target for cancer therapy

Davudian, Sadaf; Mansoori, Behzad; Shajari, Neda; Mohammadi, Ali; Baradaran, Behzad

doi:10.1016/j.gene.2016.04.040

Cited by 98 publications

(86 citation statements)

References 89 publications

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“…Even if HO-1 is associated with protection in the ECM model, this association may be lost in the absence of miR-155. Recent studies using exosomal delivery of miR-155 reported increased expression of Ho-1 mediated by miR-155 repression of Bach-1, an established transcriptional regulator of Ho-1 (40,(47)(48)(49). Collectively, these data are consistent with the hypothesis that in the absence of miR-155, there is increased Bach-1 expression, leading to decreased Ho-1 expression.…”

Section: Mir-155supporting

confidence: 78%

miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria

Barker

Kim

et al. 2017

Mol Med

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miR-155 has been shown to participate in host response to infection and neuroinflammation via negative regulation of blood-brain barrier (BBB) integrity and T cell function. We hypothesized that miR-155 may contribute to the pathogenesis of cerebral malaria (CM). To test this hypothesis, we used a genetic approach to modulate miR-155 expression in an experimental model of cerebral malaria (ECM). In addition, an engineered endothelialized microvessel system and serum samples from Ugandan children with CM were used to examine anti-miR-155 as a potential adjunctive therapeutic for severe malaria. Despite higher parasitemia, survival was significantly improved in miR-155 -/-mice versus wild-type littermate mice in ECM. Improved survival was associated with preservation of BBB integrity and reduced endothelial activation, despite increased levels of proinflammatory cytokines. Pretreatment with antagomir-155 reduced vascular leak induced by human CM sera in an ex vivo endothelial microvessel model. These data provide evidence supporting a mechanistic role for miR-155 in host response to malaria via regulation of endothelial activation, microvascular leak and BBB dysfunction in CM.

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Section: Mir-155supporting

confidence: 78%

miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria

Barker

Kim

et al. 2017

Mol Med

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“…Working as a heme-binding protein, Bach1 in resting conditions dimerizes with sMafs and binds to the ARE/Electrophile Responsive Element (EpRE) sequences preventing ARE-dependent gene transcription. Under oxidative conditions or when the concentration of heme groups increases, Bach1 is modified, displaced from ARE sequences and degraded to proteasome, allowing Nrf2 to bind [42,43]. It is important to note that many stressing conditions, particularly oxidative stressors, favor the release of heme groups from different proteins such as myoglobin, cytochromes, peroxidases, which induces Bach1-dependent HO-1 activation as a mechanism of cell adaptation.…”

Section: Molecular Mechanisms Of Ho-1 Inductionmentioning

confidence: 99%

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Nitti

Piras

Brondolo

et al. 2018

IJMS

118

107

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Heme oxygenase 1 (HO-1) up-regulation is recognized as a pivotal mechanism of cell adaptation to stress. Under control of different transcription factors but with a prominent role played by Nrf2, HO-1 induction is crucial also in nervous system response to damage. However, several lines of evidence have highlighted that HO-1 expression is associated to neuronal damage and neurodegeneration especially in Alzheimer’s and Parkinson’s diseases. In this review, we summarize the current literature regarding the role of HO-1 in nervous system pointing out different molecular mechanisms possibly responsible for HO-1 up-regulation in nervous system homeostasis and neurodegeneration.

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“…HMGA2 is a chromatin remodeling factor that promotes EMT and invasion by upregulating Snail, Slug, and Twist [14,18,110], while BACH1 is a transcription factor involved in bone metastasis of breast cancer by upregulating vital metastatic genes such as chemokine receptor type 4 ( CXCR4 ) and matrix metalloproteinase 1 ( MMP-1 ) [111]. Moreover, RKIP extends its indirect regulatory role downstream of HMGA2, in a number of additional let-7/HMGA2 targets involved in the metastatic process, as shown by gene and microRNA expression analyses performed in breast cancer cell lines [14].…”

Section: Major Rkip-induced Metastasis Suppressor Signaling Modulesmentioning

confidence: 99%

RKIP: A Key Regulator in Tumor Metastasis Initiation and Resistance to Apoptosis: Therapeutic Targeting and Impact

Zaravinos

Bonavida

Chatzaki

et al. 2018

Cancers

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RAF-kinase inhibitor protein (RKIP) is a well-established tumor suppressor that is frequently downregulated in a plethora of solid and hematological malignancies. RKIP exerts antimetastatic and pro-apoptotic properties in cancer cells, via modulation of signaling pathways and gene products involved in tumor survival and spread. Here we review the contribution of RKIP in the regulation of early metastatic steps such as epithelial–mesenchymal transition (EMT), migration, and invasion, as well as in tumor sensitivity to conventional therapeutics and immuno-mediated cytotoxicity. We further provide updated justification for targeting RKIP as a strategy to overcome tumor chemo/immuno-resistance and suppress metastasis, through the use of agents able to modulate RKIP expression in cancer cells.

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BACH1, the master regulator gene: A novel candidate target for cancer therapy

Cited by 98 publications

References 89 publications

miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria

miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

RKIP: A Key Regulator in Tumor Metastasis Initiation and Resistance to Apoptosis: Therapeutic Targeting and Impact

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