Downregulation of LAMB3 Altered the Carcinogenic Properties of Human Papillomavirus 16-Positive Cervical Cancer Cells

Author:

Wattanathavorn Warattaya12,Seki Masahide3,Suzuki Yutaka3,Buranapraditkun Supranee456,Kitkumthorn Nakarin7,Sasivimolrattana Thanayod8ORCID,Bhattarakosol Parvapan129,Chaiwongkot Arkom129ORCID

Affiliation:

1. Medical Microbiology Interdisciplinary Program, Graduate School, Chulalongkorn University, Bangkok 10330, Thailand

2. Center of Excellence in Applied Medical Virology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

3. Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa 277-8561, Chiba, Japan

4. King Chulalongkorn Memorial Hospital, Bangkok 10330, Thailand

5. Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, 1873 Rama IV Road, Chulalongkorn University, Bangkok 10330, Thailand

6. Center of Excellence in Vaccine Research and Development (Chula Vaccine Research Center—Chula VRC), Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

7. Department of Oral Biology, Faculty of Dentistry, Mahidol University, Bangkok 10400, Thailand

8. Department of Microbiology, Faculty of Public Health, Mahidol University, Bangkok 10400, Thailand

9. Department of Microbiology, Faculty of Medicine, Chulalongkorn University, 1873 Rama IV Road, Pathumwan, Bangkok 10330, Thailand

Abstract

Nearly all cervical cancer cases are caused by infection with high-risk human papillomavirus (HR-HPV) types. The mechanism of cervical cell transformation is related to the powerful action of viral oncoproteins and cellular gene alterations. Transcriptomic data from cervical cancer and normal cervical cells were utilized to identify upregulated genes and their associated pathways. The laminin subunit beta-3 (LAMB3) mRNAwas overexpressed in cervical cancer and was chosen for functional analysis. The LAMB3 was predominantly expressed in the extracellular region and the plasma membrane, which play a role in protein binding and cell adhesion molecule binding, leading to cell migration and tissue development. LAMB3 was found to be implicated in the pathway in cancer and the PI3K-AKT signaling pathway. LAMB3 knockdown decreased cell migration, invasion, anchorage-dependent and anchorage-independent cell growth and increased the number of apoptotic cells. These effects were linked to a decrease in protein levels involved in the PI3K-AKT signaling pathway and an increase in p53 protein. This study demonstrated that LAMB3 could promote cervical cancer cell migration, invasion and survival.

Funder

Thailand Science Research and Innovative Fund Chulalongkorn University

TRF Grant for a new researcher from Thailand Research Fund Grant

Chulalongkorn University Office of International Affairs Scholarship

Publisher

MDPI AG

Reference51 articles.

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