PLOD Family: A Novel Biomarker for Prognosis and Personalized Treatment in Soft Tissue Sarcoma

Abstract

Despite various treatment attempts, the heterogenous group of soft tissue sarcomata (STS) with more than 100 subtypes still shows poor outcomes. Therefore, effective biomarkers for prognosis prediction and personalized treatment are of high importance. The Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase (PLOD) gene family, which is related to multiple cancer entities, consists of three members which encode important enzymes for the formation of connective tissue. The relation to STS, however, has not yet been explored. In this study, data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases were used to analyze the role of PLOD1–3 in STS. It was found that an overexpression of PLOD family members correlates with poor prognosis, which might be due to an increased infiltration of immune-related cells in the tumor microenvironment. In STS, the expression of PLOD genes could be a novel biomarker for prognosis and a personalized, more aggressive treatment in these patients.

PLODs: Novel prognostic biomarkers and potential immunotherapy targets for head and neck squamous cell carcinoma

“…Consequently, dysregulation of PLODs could be associated with the proliferation of various tumors, including glioma, gastric, and lung cancer [ [18] , [19] , [20] , 38 ]. In addition, our previous study identified that PLODs could be regulators in lower-grade gliomas and soft tissue sarcoma, which could further support this hypothesis [ 22 , 23 ]. The third possible mechanism linking PLODs to HNSCC is the Wnt signaling pathway.…”

“…PLOD family members (PLOD1, PLOD2, and PLOD3) were shown to be associated with poor prognosis and could act as potential biomarkers or therapeutic targets for both gastric cancer and hepatocellular carcinoma [ 18 , 20 , 22 ]. Our previous studies indicated that PLOD was also associated with lower grade glioma and soft tissue sarcoma [ 22 , 23 ]. Deeper analysis showed that PLOD2 may be a crucial regulator in the invasion or metastasis of HNSCC [ 30 ].…”

“…Our previous work reported that PLOD3 likely acts as an oncogene, and overexpression of this protein may lead to various tumors [ 21 ]. In addition, changes in the expression of the PLOD family have been linked to lower grade glioma (LGG) and soft tissue sarcoma and could be a regulator of the TME [ 22 , 23 ]. Given this, we designed this study to focus on the prognostic function and molecular mechanisms of the PLOD family in HNSCC.…”