LOXL2 promotes tumor proliferation and metastasis by FAK/Src signaling in esophageal squamous cell carcinoma

Abstract

Background: Esophageal squamous cell carcinoma is the most common malignant tumor of the upper gastrointestinal tract, which is prone to metastasis and has a poor prognosis. Lysine oxidase-like protein 2 (LOXL2) is an important intracellular protein that is highly expressed in a variety of tumors, leading to reduced patient survival. Studies have shown that LOXL2 is closely associated with tumor metastasis. However, the effect of LOXL2 on the biological function of esophageal squamous cell carcinoma (ESCC) and its related mechanisms are not fully understood. This study aimed to evaluate the potential prognostic and treatment value of LOXL2 in patients with ESCC.

Results: The expression of LOXL2 was higher in ESCC tissues than in adjacent tissues. Positive LOXL2 expression was associated with poor tumor differentiation, lymph node metastases, and poor prognosis in ESCC patients. LOXL2 is an independent prognostic risk factor for ESCC. In vitro experiments showed that LOXL2 significantly promoted ESCC cell proliferation, migration, and invasion ability. LOXL2 altered the expression of the EMT marker, upregulating the mesenchymal marker (Snail) and downregulating the epithelial marker (E-cadherin). Mechanistically, LOXL2 induces EMT in esophageal squamous cell carcinoma by increasing FAK and SRC phosphorylation levels.

Conclusions: Taken together, LOXL2 regulates the FAK/Src signaling pathway to promote malignant biological behavior and EMT process in ESCC cells. LOXL2 is a marker of poor prognosis, and LOXL2 could be a promising therapeutic target for the treatment of esophageal squamous carcinoma.