Effect of Bortezomib on Global Gene Expression in PC12-Derived Nerve Cells

Łuczkowska, Karolina; Rogińska, Dorota; Ulańczyk, Zofia

doi:10.3390/ijms21030751

Cited by 12 publications

(14 citation statements)

References 45 publications

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“…Affymetrix miRNA 4.1 Array Stripes (Affymetrix, Santa Clara, CA, USA) were used for study and performed in n ¼ 3 technical replicates for each miRNA probe. Microarrays were made and analyzed according to the methods described in the previous articles [16,17].…”

Section: Mirna Analysismentioning

confidence: 99%

microRNAs as the biomarkers of chemotherapy-induced peripheral neuropathy in patients with multiple myeloma

Łuczkowska

Rogińska

Ulańczyk

et al. 2021

Leukemia & Lymphoma

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Multiple myeloma (MM) is a malignant, incurable neoplastic disease. The currently used treatment significantly improves the prognosis and extends the survival time of patients. Unfortunately, a common side effect of the therapy is peripheral neuropathy, which may lead to dose reduction or complete treatment discontinuation/modification. In this study, we examined the changes in plasma levels of circulating miRNAs in myeloma patients to define potential factors characteristic for drug-induced peripheral neuropathy (DiPN). Global miRNA expression profile in the plasma of patients with MM during treatment was determined using miRNA microarray technology. Receiver operating characteristic (ROC) analysis allowed the identification of three miRNAs (miR-22-3p; miR-23a-3p; miR-24-3p) that could be a potential biomarker of PN. The most promising results were obtained for miR-22-3p, which was characterized by ROC area under curve (AUC) ¼ 0.807. Our results suggest a relationship between the DiPN in patients with MM and the level of selected miRNAs in the plasma.

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Section: Mirna Analysismentioning

confidence: 99%

microRNAs as the biomarkers of chemotherapy-induced peripheral neuropathy in patients with multiple myeloma

Łuczkowska

Rogińska

Ulańczyk

et al. 2021

Leukemia & Lymphoma

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“…The alternative pathway of complement activation is associated with many autoimmune diseases, such as arthritis and age-related macular degeneration [ 48 ]. Levin et al demonstrated in a mouse model an increase in proteins in the complementary system including properdin and factor D, both in the peripheral and central nervous system, during neuropathic pain [ 49 ]. In our study, we were the first to demonstrate an increase in the expression of genes regulating the complement system such as CFP encoding properdin and CFD encoding Factor D in patients with neuropathy.…”

Section: Discussionmentioning

confidence: 99%

The Potential Role of Proinflammatory Cytokines and Complement Components in the Development of Drug-Induced Neuropathy in Patients with Multiple Myeloma

Łuczkowska

Rutka

Rogińska

et al. 2021

JCM

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The launch of novel chemotherapeutic agents—in particular, proteasome inhibitors and immunomodulatory drugs—dramatically changed multiple myeloma (MM) therapy, improving the response rate and prolonging progression-free survival. However, none of the anti-MM drugs are deprived of side effects. Peripheral neuropathy (PN) seems to be one of the most pressing problems. Despite extensive research in this area, the pathogenesis of drug-induced peripheral neuropathy (DiPN) has not yet been fully elucidated. In the present study, we aimed to assess the potential relationship between proinflammatory factors and the development of PN in MM patients with particular emphasis on the application of VTD (bortezomib, thalidomide, dexamethasone) regimen. Our analysis identified increased concentrations of CCL2, IL-1β, and IFN-γ in plasma of MM patients during treatment, both with and without symptoms of PN, compared with untreated neuropathy-free MM patients. At the same time, the plasma concentration of IL-1β in patients with neuropathy was significantly increased compared with patients without PN before and during treatment. Moreover, the results were enhanced at the transcript level by performing global mRNA expression analysis using microarray technology. The most significant changes were observed in the expression of genes responsible for regulating immunological and apoptotic processes. An in-depth understanding of the mechanisms responsible for the development of DiPN might in the future reduce the incidence of PN and accelerate diagnosis, allowing the choice of neuropathy-free treatment strategies for MM.

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“…In previous studies, miR-152-3p was discovered to modulate cell proliferation and invasion by targeting forkhead box F1 (FOXF1) in keloid fibroblasts [ 48 ]. The miR-152-3p/Gadd45 correlation is also investigated in PC12-Derived nerve cells [ 49 ]. To explore the downstream molecule of miR-152-3p, mRNAs binding with miR-152-3p were predicted using the starBase, and DDX6 was finally selected for further study due to its increased expression mediated by miR-152-3p inhibition in cells.…”

Section: Discussionmentioning

confidence: 99%

miR-152-3p aggravates vascular endothelial cell dysfunction by targeting DEAD-box helicase 6 (DDX6) under hypoxia

Zhao

et al. 2021

Bioengineered

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Stroke is a main cause of disability and death worldwide, and ischemic stroke accounts for most stroke cases. Recently, microRNAs (miRNAs) have been verified to play critical roles in the development of stroke. Herein, we explored effects of miR-152-3p on vascular endothelial cell functions under hypoxia. Human umbilical vein endothelial cells (HUVECs) were treated with hypoxia to mimic cell injury in vitro. Reverse transcription quantitative polymerase chain reaction revealed that miR-152-3p exhibited high expression in HUVECs treated with hypoxia. The inhibition of miR-152-3p reversed hypoxia-induced decrease in cell viability and the increase in angiogenesis, according to the results of cell counting kit-8 assays and tube formation assays. miR-152-3p inhibition reversed the increase in endothelial cell permeability mediated by hypoxia, as shown by endothelial cell permeability in vitro assays. In addition, the increase in protein levels of angiogenetic markers and the decrease in levels of tight junction proteins induced by hypoxia were reversed by miR-152-3p inhibition. Mechanistically, miR-152-3p directly targets 3untranslated region of DEAD-box helicase 6 (DDX6), which was confirmed by luciferase reporter assays. DDX6 is lowly expressed in HUVECs under hypoxic condition, and mRNA expression and protein level of DDX6 were upregulated in HUVECs due to miR-152-3p inhibition. Rescue assays showed that DDX6 knockdown reversed effects of miR-152-3p on cell viability, angiogenesis and endothelial permeability. The results demonstrated that miR-152-3p aggravates vascular endothelial cell dysfunction by targeting DDX6 under hypoxia.

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Effect of Bortezomib on Global Gene Expression in PC12-Derived Nerve Cells

Cited by 12 publications

References 45 publications

microRNAs as the biomarkers of chemotherapy-induced peripheral neuropathy in patients with multiple myeloma

microRNAs as the biomarkers of chemotherapy-induced peripheral neuropathy in patients with multiple myeloma

The Potential Role of Proinflammatory Cytokines and Complement Components in the Development of Drug-Induced Neuropathy in Patients with Multiple Myeloma

miR-152-3p aggravates vascular endothelial cell dysfunction by targeting DEAD-box helicase 6 (DDX6) under hypoxia

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