The overexpression of the
enzymes involved in the degradation of
procollagen lysine is correlated with various
tumor entities.
Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 3 (PLOD3) expression was found to be correlated to the progression and migration of
cancer cells in gastric, lung and
prostate cancer. Here, we analyzed the gene expression,
protein expression, and the clinical parameters of survival across 33
cancers based on the Clinical Proteomic
Tumor Analysis Consortium (CPTAC), function annotation of the mammalian genome 5 (FANTOM5), Gene Expression Omnibus (GEO), Genotype-Tissue Expression (GTEx), Human
Protein Atlas (HPA) and The
Cancer Genome Atlas (TCGA) databases. Genetic alteration, immune infiltration and relevant cellular pathways were analyzed in detail. PLOD3 expression negatively correlated with survival periods and the infiltration level of CD8+ T cells, but positively correlated to the infiltration of cancer associated fibroblasts in diverse
cancers. Immunohistochemistry in colon
carcinomas,
glioblastomas, and
soft tissue sarcomas further confirm PLOD 3 expression in human
cancer tissue. Moreover, amplification and mutation accounted for the largest proportion in esophageal
adenocarcinoma and uterine corpus
endometrial carcinoma, respectively; the copy number alteration of PLOD3 appeared in all
cancers from TCGA; and molecular mechanisms further proved the effect of PLOD3 on
tumorigenesis. In particular, PLOD3 expression appears to have a
tumor immunological effect, and is related to multiple immune cells. Furthermore, it is also associated with
tumor mutation burden and
microsatellite instability in various
tumors. PLOD3 acts as an inducer of various
cancers, and it could be a potential
biomarker for prognosis and targeted treatment.