Podoplanin, a Potential Therapeutic Target for Nasopharyngeal Carcinoma

Author:

Hsu Yen-Bin12ORCID,Huang Chi-Ying F.23,Lin Kuan-Ting4,Kuo Yu-Lun5,Lan Ming-Chin67ORCID,Lan Ming-Ying18ORCID

Affiliation:

1. Department of Otolaryngology-Head and Neck Surgery, Taipei Veterans General Hospital, Taipei 11217, Taiwan

2. Institute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan

3. Institute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, Taiwan

4. Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA

5. Biotools, Co., Ltd, New Taipei City 22175, Taiwan

6. Department of Otolaryngology-Head and Neck Surgery, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23142, Taiwan

7. School of Medicine, Tzu Chi University, Hualien 97004, Taiwan

8. School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan

Abstract

Introduction. The role of podoplanin (PDPN) in nasopharyngeal carcinoma (NPC) is still unknown. The aims of this study were to investigate the expression and role of PDPN in NPC cells.Materials and Methods. Immunofluorescence staining and functional tests were used to determine the effects of PDPN knockdown by siRNA in TW01 NPC cells. Microarray analysis was conducted to identify genes regulated by PDPN. The molecular mechanism of PDPN on NPC cells was further determined by Ingenuity Pathways Analysis (IPA).Results. PDPN was expressed in most TW01 NPC cells. PDPN knockdown by siRNA decreased NPC cell proliferation, migration, and invasion. The microarray data showed 63 upregulated genes and 12 downregulated genes following PDPN knockdown. The top 5 most upregulated genes analyzed by IPA were IFI27, IFI44L, IFI6, OAS1, and TRIM22, and the most relevant pathway was the interferon signaling pathway.Conclusions. To the best of our knowledge, this is the first report to show that knocking down PDPN leads to suppression of NPC cell proliferation, migration, and invasion. Our results suggest that PDPN may serve as a potential chemotherapeutic target for NPC treatment in the future.

Funder

Taipei Veterans General Hospital

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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