Research Paper Volume 16, Issue 10 pp 9204—9215

DKK2 promotes the progression of oral squamous cell carcinoma through the PI3K/AKT signaling pathway

Wenbo Guo1,2, *, , Yun Qu3, *, , Yang Yu1, , Xueming Li1, , Zhuang Liang1, , Zhaoqi Wang1, , Tenglong Hu1, , Shan Zhou3, ,

  • 1 Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Harbin Medical University, School of Stomatology, Harbin 150001, Heilongjiang, China
  • 2 Key Laboratory of Hepatosplenic Surgery, Ministry of Education, Harbin 150001, Heilongjiang, China
  • 3 Department of Orthodontics, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China
* Equal contribution and co-first authors

Received: November 29, 2023       Accepted: March 29, 2024       Published: May 24, 2024      

https://doi.org/10.18632/aging.205864
How to Cite

Copyright: © 2024 Guo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: This study aimed to investigate the impact of Dickkopf 2 (DKK2) on the progression of oral squamous cell carcinoma (OSCC) and explore its role in the PI3K/AKT signaling transduction pathway.

Materials and Methods: The study initially examined the expression of the DKK2 gene in OSCC tissues and normal tissues. Simultaneously, the expression of DKK2 in HOK cells and OSCC cells was verified, and changes in DKK2 expression under hypoxic conditions were detected. DKK2 overexpression and knockdown were performed in SCC-15 and CAL-27 cells. Subsequently, the effects of DKK2 on the proliferation, migration and invasion of OSCC were detected. Western blotting was employed to detect the expression of key proteins in the DKK2/PI3K/AKT signaling axis before and after transfection, and further explore the relevant molecular mechanisms.

Results: Compared to normal tissues, DKK2 expression was elevated in OSCC tissues. The expression of DKK2 in the SCC-15 and CAL-27 cell lines was higher than that in HOK cells, and hypoxic conditions could promote DKK2 expression. DKK2 overexpression promoted cell proliferation, migration, and invasion, while DKK2 knockdown inhibited these processes. DKK2 overexpression activated the PI3K/AKT pathway, while DKK2 knockdown suppressed this pathway.

Conclusion: This study suggests that hypoxic conditions enhance the expression of DKK2 in OSCC. DKK2 regulates the proliferation, migration, and invasion of OSCC through the PI3K/AKT signaling pathway.

Abbreviations

DKK2: Dickkopf related protein 2; OSCC: Oral squamous cell carcinoma; PI3K/AKT: PhosphoInositide3-Kinase/Protein kinase B; HNSCC: Head and neck squamous cell carcinoma.