Journals / ONCOLOGIE / Vol.23, No.3 / doi:10.32604/oncologie.2021.017786


Overexpression of lnc-ERP44-3:6 Causes Cell Death and Sensitivity to Cisplatin in Breast Cancer Cell Lines

Elda A. Flores-Contreras1, Everardo González-González2,3, Ana I. Zarazúa-Niño1, Elsa N. Garza-Treviño1, Natalia Martínez-Acuña1, Viviana C. Zomosa-Signoret4, Román Vidaltamayo4, Gerardo E. Muñoz-Maldonado5, Raquel Garza-Guajardo6, Manuel de J. García-Solís7, Alejandro Abarca-Blanco3, Ana M. G. Rivas-Estilla1, Carlos Córdova-Fletes1,*
1 Departamento de Bioquímica y Medicina Molecular, Facultad de Medicina, Universidad Autónoma de Nuevo León, Nuevo León, 64460, Mexico
2 Centro de Biotecnología-FEMSA, Tecnológico de Monterrey, Nuevo León, 64849, Mexico
3 Delee Corp, Mountain View, CA 94041, USA
4 Department of Basic Science, School of Medicine, Universidad de Monterrey, Nuevo León, 66238, Mexico
5 Department of General Surgery, Hospital Universitario, Dr. José Eleuterio González, Universidad Autónoma de Nuevo León, Nuevo León, 66460, Mexico
6 Department of Pathology and Cytopathology, Facultad de Medicina, Dr. José Eleuterio Gonzáles, Universidad Atónoma de Nuevo León, Nuevo León, 66460, Mexico
7 Clínica de Mama, Hospital Metropolitano, Dr. Bernardo Sepúlveda, Secretaría de Salud, Nuevo León, 66480, Mexico
* Corresponding Author: Carlos Córdova-Fletes. Email:
Received 06 June 2021; Accepted 14 August 2021; Issue published 26 September 2021


Breast cancer (BC) is one of the leading causes of death in women worldwide. A major challenge in BC is chemoresistance, which is often modulated by epigenetic regulators such as long non-coding RNAs (lncRNAs). Because these regulator lncRNAs may play diverse roles, determining their specific pathways and/or functions is crucial to identify possible biomarkers and/or therapeutic targets for BC. In this study, we used gene expression microarrays in order to identify lncRNAs related to the BC biology. We found, among six differentially expressed (DE) lncRNAs, that the expression of lnc-ERP44-3:6 was consistently down-regulated in all breast tumor tissues compared to normal adjacent tissues of BC patients from northeastern Mexico. Since the role of lnc-ERP44-3:6 remains unknown in BC, we induced its transient overexpression in three different BC cell lines (i.e., MCF10A, MCF-7, and HCC1395) by transfection in order to elucidate its potential downstream effects. Remarkably, our results showed a significant increase in cell death and chemosensitivity to cisplatin at 48 h post-transfection (p < 0.01). In addition, we observed that GAPDH and FAS were up-regulated following the overexpression of lnc-ERP44-3:6. As GAPDH and FAS promote apoptosis in cancer, our findings suggest that the lnc-ERP44-3:6 overexpression induces cell death possibly via up-regulation of one or both genes in BC cell lines. To the best of our knowledge, this is the first study evaluating the overexpression of lnc-ERP44-3:6 and providing insights about its role in BC cells, which suggests that this lncRNA may be an interesting candidate as a potential therapeutic target for BC in our population. However, further studies would be needed to clarify the mechanisms by which an overexpression of lnc-ERP44-3:6 causes both cell death and chemosensitivity to cisplatin.


Breast cancer; lncRNA; lnc-ERP44-3:6; biomarker; therapeutic target; chemoresistance; tumor suppressor
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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