Guest editorial: understanding the pathogenesis and the evolving treatment paradigm for multiple myeloma in the era of novel agents

Abe, Masahiro

doi:10.1007/s12185-011-0950-4

Cited by 5 publications

(2 citation statements)

References 17 publications

(19 reference statements)

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“…Such upregulation represents an intrinsic defense mechanism to maintain cellular homeostasis and enhance cell survival [8]. In some cancer cells, HO-1 is considered to play a major role as an essential survival factor, protecting against chemotherapy-induced reactive oxygen species (ROS) increase [9][10][11][12][13][14]. Interestingly, the role of HO-1 in cancer cells has been shown to be cell-specific since in some tumors its upregulation has been shown to be associated with cell cycle arrest and/or death whereas in other malignancies it was associated with tumor progression and survival [15,16].…”

Section: Introductionmentioning

confidence: 99%

Effect of Lipoic Acid on the Biochemical Mechanisms of Resistance to Bortezomib in SH-SY5Y Neuroblastoma Cells

et al. 2017

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Neuroblastoma (NB) is an extracranial solid cancer and the most common cancer in infancy. Despite the standard treatment for NB is based on the combination of chemotherapeutic drugs such as doxorubicin, vincristine, cyclophosphamide, and cisplatin, chemoresistance occurs over the time. The aim of the present research was to evaluate the effect of bortezomib (BTZ) (50 nM) on NB cell viability and how lipoic acid (ALA) (100 μM) modifies pharmacological response to this chemotherapeutic agent. Cell viability was assessed by ATP luminescence assay whereas expression of oxidative stress marker (i.e., heme oxygenase-1) and endoplasmic reticulum stress proteins was performed by real-time PCR, western blot, and immunofluorescence. Our data showed that BTZ treatment significantly reduced cell viability when compared to untreated cultures (about 40%). Interestingly, ALA significantly reduced the efficacy of BTZ (about 30%). Furthermore, BTZ significantly induced heme oxygenase-1 as a result of increased oxidative stress and such overexpression was prevented by concomitant treatment with ALA. Similarly, ALA significantly reduced BTZ-mediated endoplasmic reticulum stress as measured by reduction in BiP1 and IRE1α, ERO1α, and PDI expression. In conclusion, our data suggest that BTZ efficacy is dependent on cellular redox status and such mechanisms may be responsible of chemoresistance to this chemotherapeutic agent.

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Section: Introductionmentioning

confidence: 99%

Effect of Lipoic Acid on the Biochemical Mechanisms of Resistance to Bortezomib in SH-SY5Y Neuroblastoma Cells

et al. 2017

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“…HO-1 is widely expressed at low levels in several tissues, where it catalyzes the degradation of heme to biliverdin, free ferrous iron, and CO, playing a major role in the cellular response to oxidative stress [ 8 ]. Within the tumor context, this protein has been previously described as an oncogenic factor eventually protecting cancer cells by scavenging reactive oxygen species (ROS) and in turn increasing upon chemotherapeutic treatments [ 9 , 10 , 11 , 12 , 13 , 14 ]. In melanoma cells, HO-1 overexpression increases viability, proliferation, and angiogenetic potential, eventually increasing metastasis formation rate and hampering tumor-bearing mouse survival [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Heme Oxygenase-1 Overexpression Promotes Uveal Melanoma Progression and Is Associated with Poor Clinical Outcomes

et al. 2022

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Uveal melanoma (UM) is the most common primary intraocular tumor in adults. To date, the main strategies to counteract its progression consist of focal radiation on the tumor site and ocular enucleation. Furthermore, many UM patients develop liver metastasis within 10 years following diagnosis, eventually resulting in a poorer prognosis for those patients. Dissecting the molecular mechanism involved in UM progression may lead to identify novel prognostic markers with significative clinical applications. The aim of the present study was to evaluate the role of Heme Oxygenase 1 (HO-1) in regulating UM progression. UM cell lines (92.1) were treated with Hemin (CONC e time), a strong inducer of HO-1, and VP13/47, a selective inhibitor of its enzymatic activity. Interestingly, our results showed an enhanced 92.1 cellular proliferation and wound healing ability following an HO-1 increase, overall unveiling the role played by this protein in tumor progression. Similar results were obtained following treatment with two different CO releasing molecules (CORM-3 and CORM-A1). These results were further confirmed in a clinical setting using our UM cohort. Our results demonstrated an increased median HO-1 expression in metastasizing UM when compared to nonmetastasizing patients. Overall, our results showed that HO-1 derived CO plays a major role in UM progression and HO-1 protein expression may serve as a potential prognostic and therapeutical factor in UM patients.

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The Heme Oxygenase System in Hematological Malignancies

Volti

Tibullo

Vanella

et al. 2017

Antioxidants & Redox Signaling

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Guest editorial: understanding the pathogenesis and the evolving treatment paradigm for multiple myeloma in the era of novel agents

Cited by 5 publications

References 17 publications

Effect of Lipoic Acid on the Biochemical Mechanisms of Resistance to Bortezomib in SH-SY5Y Neuroblastoma Cells

Effect of Lipoic Acid on the Biochemical Mechanisms of Resistance to Bortezomib in SH-SY5Y Neuroblastoma Cells

Heme Oxygenase-1 Overexpression Promotes Uveal Melanoma Progression and Is Associated with Poor Clinical Outcomes

The Heme Oxygenase System in Hematological Malignancies

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