2. Academic Validation
  3. KIFC3 promotes the proliferation, migration and invasion of non-small cell lung cancer through the PI3K/AKT signaling pathway

KIFC3 promotes the proliferation, migration and invasion of non-small cell lung cancer through the PI3K/AKT signaling pathway

  • Sci Rep. 2024 Sep 3;14(1):20471. doi: 10.1038/s41598-024-71602-0.
Yue Ma 1,  Yao Zhang 2,  Xizi Jiang 2,  Jingqian Guan 3,  Huanxi Wang 3,  Jiameng Zhang 2,  Yue Tong 2,  Xueshan Qiu 4,  Renyi Zhou 5
Affiliations

Affiliations

  • 1 Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, China.
  • 2 Department of Pathology, China Medical University, 77 Puhe Road, North Shenyang New Area, Shenyang, 110122, Liaoning, China.
  • 3 Department of Pathology, Shengjing Hospital of China Medical University, Shenyang, China.
  • 4 Department of Pathology, China Medical University, 77 Puhe Road, North Shenyang New Area, Shenyang, 110122, Liaoning, China. xsqiu@cmu.edu.cn.
  • 5 Department of Orthopedics, First Hospital of China Medical University, No.155 Nan Jing North Street, Shenyang, 110001, Liaoning, China. ryzhou@cmu.edu.cn.
PMID: 39227687 DOI: 10.1038/s41598-024-71602-0
Abstract

KIFC3 is a member of the Kinesin superfamily proteins (KIFs). The role of KIFC3 in non-small cell lung Cancer (NSCLC) is unknown. This study aimed to elucidate the function of KIFC3 in NSCLC and the underlying mechanism. Immunohistochemistry indicated that KIFC3 was highly expressed in NSCLC tissues and correlated with the degree of differentiation, tumor size, lymph node metastasis and TNM stage. MTT, colony formation and Transwell assays demonstrated that KIFC3 overexpression promoted the proliferation, migration and invasion of NSCLC cells in vitro, while KIFC3 knockdown led to the opposite results. The protein expression levels of PI3Kp85α and p-Akt were increased after KIFC3 overexpression, meanwhile the downstream protein expression levels such as cyclin D1, CDK4, CDK6, RhoA, RhoC and MMP2 were increased. This promotion effect could be inhibited by a specific inhibitor of the PI3K/Akt pathway, LY294002. Co-immunoprecipitation assays confirmed the interaction between endogenous/exogenous KIFC3 and PI3Kp85α. Tumor formation experiments in nude mice confirmed that KIFC3 overexpression promoted the proliferation, migration and invasion of NSCLC cells in vivo and performed its biological function through the PI3K/Akt signaling pathway.In conclusion, KIFC3 promotes the malignant behavior of NSCLC cells through the PI3K/Akt signaling pathway.

Keywords

KIFC3; Migration; Non-small cell lung cancer; PI3K/Akt signaling pathway; Proliferation.

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