ABSTRACT
Objective:
This study aims to establish a theoretical
foundation for the clinical
treatment of
lung cancer by investigating the regulatory
role of CRABP2 in the ROS/Src signaling pathway, specifically in accelerating the migration and
metastasis of
lung cancer.
Methods:
Lung cancer mouse models were established using BALB/c-nu
mice, randomly assigned to the
control group (NC group) and the experimental group (mimic group).
Tumor volume was precisely observed. The impact of CRABP2 on
lung cancer migration and
metastasis was analyzed through
hematoxylin and
eosin (H&E)
staining and histochemical
staining observation.
Protein expression
analysis was employed to assess CRABP2, ESR1, NOX1, NOX4, p-Src, and p-FAK levels, shedding
light on the underlying mechanism. CRABP2's influence on
lung cancer migration and
metastasis was further investigated using scratch and Transwell experiments.
Results:
The findings revealed that the mimic group, with enhanced CRABP2 expression, exhibited a higher proliferation rate and increased migration and
metastasis capabilities in
lung cancer.
Protein expression
analysis demonstrated that CRABP2 and ESR1 positively influenced the ROS/Src pathway, promoting
lung cancer migration and
metastasis. Scratch and Transwell's experiments supported the fact that CRABP2 significantly accelerated
lung cancer migration and
metastasis.
Conclusions:
CRABP2
plays a crucial
role in expediting
lung cancer migration and
metastasis by upregulating ESR1 expression, consequently activating the ROS/Src pathway. This study introduces a novel
therapeutic avenue for the clinical
treatment of
lung cancer, offering a theoretical framework for advancing
lung cancer treatment strategies.