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Figure S2 from TBX3 Promotes Cervical Cancer Proliferation and Migration via HPV E6 and E7 Signaling

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posted on 2023-04-03, 08:40 authored by Saif F. Khan, Carly A. Burmeister, David J. Scott, Musalula Sinkala, Amsha Ramburan, Hue-Tsi Wu, Georgia Schäfer, Arieh A. Katz, Sharon Prince

HPV18 E6 and E7 oncogene mRNA expression in the E6, E7 and E6/E7 stably transfected cells compared to the wild type and empty vector controls.

Funding

Cancer Association of South Africa (CANSA)

National Research Foundation (NRF)

South African Medical Research Council (SAMRC)

International Centre for Genetic Engineering and Biotechnology (ICGEB)

University of Cape Town (UCT)

Poliomyelitis Research Foundation (PRF)

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ARTICLE ABSTRACT

Cervical cancer is a leading cause of cancer-related deaths in women globally and 99% of cases are caused by persistent infection with high-risk strains of the human papillomavirus (HPV). The HPV oncoproteins E6 and E7 establish the cancer phenotype by cooperating with host proteins and identifying them may have important therapeutic benefits. T-box transcription factor 3 (TBX3) is a critical developmental regulator, and when it is overexpressed postnatally, it contributes to several cancers, but little is known about its expression and role in cervical cancer. The current study shows that TBX3 is upregulated in cervical cancer cell lines as well as precancerous and cervical cancer patient tissue and is associated with larger and more invasive tumors. Knockdown and overexpression cell culture models show that TBX3 promotes HPV-positive cell proliferation, migration, and spheroid growth; however, TBX3 inhibits these processes in HPV-negative cells. Importantly, we show that the tumor promoting activity of TBX3 in cervical cancer is dependent on E6/E7. In summary, our study highlights the importance of TBX3 as a cooperating partner of E6/E7 in HPV-positive cervical cancer and identifies TBX3 as a potential therapeutic target to treat this neoplasm.

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    Molecular Cancer Research

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