10.3389/fonc.2018.00199.s001
Sabrina Piras
Sabrina
Piras
Anna L. Furfaro
Anna L.
Furfaro
Rocco Caggiano
Rocco
Caggiano
Lorenzo Brondolo
Lorenzo
Brondolo
Silvano Garibaldi
Silvano
Garibaldi
Caterina Ivaldo
Caterina
Ivaldo
Umberto M. Marinari
Umberto
M. Marinari
Maria A. Pronzato
Maria
A. Pronzato
Raffaella Faraonio
Raffaella
Faraonio
Mariapaola Nitti
Mariapaola
Nitti
data_sheet_1_microRNA-494 Favors HO-1 Expression in Neuroblastoma Cells Exposed to Oxidative Stress in a Bach1-Independent Way.docx
Frontiers
2018
heme oxygenase 1
neuroblastoma
miR-494
oxidative stress
Bach1
2018-06-13 04:17:27
Dataset
https://frontiersin.figshare.com/articles/dataset/data_sheet_1_microRNA-494_Favors_HO-1_Expression_in_Neuroblastoma_Cells_Exposed_to_Oxidative_Stress_in_a_Bach1-Independent_Way_docx/6505361
<p>Heme oxygenase 1 (HO-1) is crucially involved in cell adaptation to oxidative stress and has been demonstrated to play an important role in cancer progression and resistance to therapies. We recently highlighted that undifferentiated neuroblastoma (NB) cells are prone to counteract oxidative stress through the induction of HO-1. Conversely, differentiated NB cells were more sensitive to oxidative stress since HO-1 was scarcely upregulated. In this work, we investigated the role played by miR-494, which has been proved to be involved in cancer biology and in the modulation of oxidative stress, in the upregulation of HO-1. We showed that NB differentiation downregulates miR-494 level. In addition, endogenous miR-494 inhibition in undifferentiated cells impairs HO-1 induction in response to exposure to 500 µM H<sub>2</sub>O<sub>2</sub>, reducing the number of viable cells. The analysis of Bach1 expression did not reveal any significant modifications in any experimental conditions tested, proving that the impairment of HO-1 induction observed in cells treated with miR-494 inhibitor and exposed to H<sub>2</sub>O<sub>2</sub> is independent from Bach1. Our results underline the role played by miR-494 in favoring HO-1 induction and cell adaptation to oxidative stress and contribute to the discovery of new potential pharmacological targets to improve anticancer therapies.</p>