KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway

Guancheng Liu; Gengming Cai; Xiaosong He; Donghai Huang; Gangcai Zhu; Changhan Chen; Xin Zhang

doi:10.21037/tcr.2019.09.38

KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway

Transl Cancer Res. 2019 Oct;8(6):2252-2263. doi: 10.21037/tcr.2019.09.38.

Authors

Guancheng Liu^{1

2}, Gengming Cai³, Xiaosong He², Donghai Huang¹, Gangcai Zhu⁴, Changhan Chen¹, Xin Zhang¹

Affiliations

¹ Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, Changsha 410008, China.
² Department of Otolaryngology Head and Neck Surgery, Affiliated Hospital of Guilin Medical University, Guilin 541001, China.
³ Department of Otolaryngology Head and Neck Surgery, First Affiliated Hospital of Quanzhou, Fujian Medical University, Quanzhou 362000, China.
⁴ Department of Otolaryngology Head and Neck Surgery, The Second Xiangya Hospital, Central South University, Changsha 410010, China.

Abstract

Background: KIF18A has been shown to participate in the development of various human malignancies. However, the role of KIF18A in head and neck squamous cell carcinoma (HNSCC) remains unknown. This study investigated the function of KIF18A in HNSCC as well as its possible mechanisms.

Methods: In this study, we conducted in vitro experiments. First, we examined the effect of KIF18A on Tu686 and 6-10B cells via determining cell viability, colony formation ability and cell motility. And then, we examined that whether the carcinogenic effect of KIF18A is associated with Akt activation.

Results: Our current study demonstrated that KIF18A expression was increased in HNSCC patients and its cell lines. Knockdown and overexpression of KIF18A in HNSCC cells indicated that KIF18A promoted cancer cell proliferation, invasion and migration. Moreover, these bioactivity changes in HNSCC cells were accompanied by enhanced Vimentin expression and suppressed E-cadherin expression induced by KIF18A. Further mechanistic analysis revealed that the carcinogenic effect of KIF18A is associated with Akt activation, and blocking the activity of Akt reversed the malignant progression caused by KIF18A overexpression in HNSCC cells.

Conclusions: Together, our study reveals that KIF18A accelerates the progression of HNSCC and that targeting KIF18A may be a potential therapeutic strategy for the HNSCC.

Keywords: Akt; KIF18A; head and neck squamous cell carcinoma (HNSCC); invasion; migration; proliferation.