Published online Jul 15, 2022. doi: 10.4251/wjgo.v14.i7.1239
Peer-review started: November 18, 2021
First decision: January 12, 2022
Revised: January 26, 2022
Accepted: March 26, 2022
Article in press: March 26, 2022
Published online: July 15, 2022
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies. The mechanism of ESCC is still unclear.
Kinesin family member (KIF)C3 has microtubule motor activity and may be involved in mitotic progression. KIFC3 was also shown to be involved in cell invasion and migration, as well as in survival, in hepatocellular carcinoma.
To elucidate the role of KIFC3 in ESCC and the underlying mechanisms.
The expression of KIFC3 was evaluated in ESCC tissues and normal tissues. In addition, KIFC3 knockdown and KIFC3-overexpressing cell lines were constructed and then colony formation, EdU assays, cell cycle analysis, Transwell assays, and western blotting were performed to explore the underlying mechanisms of action. A xenograft tumor model in nude mice was used to verify the role of KIFC3 in tumorigenesis.
We showed that KIFC3 was upregulated in ESCC tissues and was associated with poor prognosis. KIFC3 promoted cell proliferation, mitosis progression, migration and invasion. In addition, KIFC3 knockdown suppressed ESCC tumorigenesis in an in vivo model. Mechanistically, we validated the involvement of KIFC3 β-catenin signaling and epithelial–mesenchymal transition (EMT) in ESCC progression.
We found that KIFC3 was overexpressed in ESCC, and the expression of this protein was associated with prognosis in ESCC patients. Furthermore, KIFC3 promoted proliferation, migration, and invasion of ESCC via β-catenin signaling and EMT.
Although the detailed mechanism underlying the effect of KIFC3 in promoting ESCC progression should be studied more carefully in our next research, we believe our research strongly suggests that KIFC3 may be a potential new therapeutic target for ESCC treatment.