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

Abstract

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. 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. 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. Our study provides insights into the expression and function of FKBP10 in the microenvironment of gastric cancer.