YBX1 promotes tumor progression via the PI3K/AKT signaling pathway in laryngeal squamous cell carcinoma

Background: Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly seen malignancies of the head and neck, with increasing incidence and mortality. The Y-box-binding protein 1 (YBX1) is a type of oncoprotein which is related to the malignant phenotype of many cancers. It is reported that YBX1 could regulate tumorigenesis, recurrence, and metastasis in multiple cancers. However, little is known about its carcinogenic function and mechanism in LSCC. Methods: Firstly, Through Oncomine StarBase, we found that the YBX1 mRNA level was increased in a variety of cancer tissues, including in the LSCC, compared with normal tissues. We silenced YBX1 in LSCC cells using short hairpin RNAs (shRNAs). Secondly, the biological function of YBX1 in LSCC cells was examined by the Cell Counting Kit-8 (CCK-8) assay, flow cytometry, the wound healing assay, and the transwell assay. Thirdly, the correlation between YBX1 and the PI3K/AKT pathway was verified by the western blot assay. Results: Expression of YBX1 is higher in a variety of cancer tissues, especially in the head and neck cancers. After transfected with lentiviral vectors, the expression of YBX1 was significantly silenced. Functionally, low expression of YBX1 promoted LSCC cell apoptosis and inhibited LSCC cell proliferation, migration, and invasion. The transfection of sh-YBX1 resulted in an obvious decrease in PI3K/AKT signaling molecules in LSCC cells. Conclusions: We demonstrated that YBX1 could promote LSCC cell progression through the PI3K/AKT pathway, providing new insights into a potential biomarker and target for LSCC treatment.

Automated summary

YBX1 is overexpressed in various cancer tissues, especially in head and neck cancers. Silencing YBX1 promotes apoptosis and inhibits proliferation, migration, and invasion of LSCC cells, possibly through the PI3K/AKT pathway. This study provides new insights into the potential use of YBX1 as a biomarker and therapeutic target for LSCC.