The integration of bulk and single-cell sequencing data revealed the function of FKBP10 in the gastric cancer microenvironment.

ABSTRACT

Background: Due to the implementation of individualized treatment, the majority of gastric cancer patients have a favorable prognosis, but advanced gastric cancer with recurrence and distant metastasis still plagues some patients. As a member of the FK506-binding protein (FKBP65) family, there is growing evidence that FKBP10 plays a crucial role in tumorigenesis. However, the role of FKBP10 in the tumor microenvironment (TME) has been a prominent issue. Methods: The FKBP10 knockdown efficiency in gastric cancer cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Wound healing and transwell analysis were performed to detect variations in cell invasion and migration. We integrated single-cell and bulk sequencing data to further elaborate the impact of FKBP10 and FKBP10-coexpressed genes (FCGs) in the TME via a variety of bioinformatics approaches. Results: Here, we found that FKBP10 knockdown inhibited cell invasion and metastasis. FKBP10 was chiefly expressed in inflammatory cancer-associated fibroblasts (iCAFs), and FCGs principally mediated alterations in extracellular matrix (ECM) organization. Besides, according to nine prognosis-related FCGs, two disparate clusters were identified, and differences in tumor immune infiltration characteristics and immunotherapy response between different clusters were investigated. Conclusions: Our study provides insights into the expression and function of FKBP10 in the microenvironment of gastric cancer.