AUTHOR=Gupta Ishita , Jabeen Ayesha , Vranic Semir , Al Moustafa Ala-Eddin , Al-Thawadi Hamda 

TITLE=RETRACTED: Oncoproteins of High-Risk HPV and EBV Cooperate to Enhance Cell Motility and Invasion of Human Breast Cancer Cells via Erk1/Erk2 and β-Catenin Signaling Pathways

JOURNAL=Frontiers in Oncology

VOLUME=Volume 11 - 2021

YEAR=2021

URL=https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2021.630408

DOI=10.3389/fonc.2021.630408

ISSN=2234-943X

ABSTRACT=Breast cancer is a leading cause of death in women around the world. Most of breast cancer-related deaths are a result of complications from the metastatic spread. Several recent studies reported that high-risk human papillomaviruses (HPVs) and Epstein-Barr virus (EBV) are co-present in different types of human carcinomas including breast; however, the cooperative effects between high-risk HPVs and EBV oncoproteins in human breast cancer have not been investigated yet. Thus, we herein explored the cooperation outcome between E6/E7 and LMP1 oncoproteins of high-risk HPV type 16 and EBV, respectively, in two human breast cancer cell lines, MCF7 and MDA-MB-231. Our data revealed that E6/E7 and LMP1 oncoproteins cooperation stimulate cell proliferation and deregulate cell cycle progression of human breast cancer cells; in parallel, we noted that E6/E7/LMP1 incite colony formation of both cell lines. More significantly, our results point out that co-expression of E6/E7 and LMP1 oncoproteins enhances cell motility and invasion of MCF7 and MDA-MB-231 cell lines; this is accompanied by deregulation of epithelial-mesenchymal transition biomarkers including E-cadherin, -catenin, fascin and vimentin. The molecular pathway analysis of HPV and EBV oncoproteins cooperation shows that it can enhance the phosphorylation of Erk1/Erk2 in addition to -catenin, which could be behind the effect of this cooperation in our cell models. The study clearly suggests that high-risk HPV and EBV co-infection can play an important role in breast cancer progression via Erk1/Erk2 and β-catenin signaling pathways.