Abstract
Tumor protein D52-like 2 (TPD52L2) belongs to the members of the TPD52 family. TPD52L2 was reported to regulate proliferation and apoptosis in cancer cells. However, its role in lung adenocarcinoma (LUAD) was uncertain. We evaluated the expression, methylation, copy number alteration, and prognostic significance of TPD52L2 using RNA-seq data from The Cancer Genome Atlas (TCGA). Enrichment analysis of TPD52L2 was conducted using the R package “clusterProfiler.” We further assessed the association between TPD52L2 and immune cell infiltration level, immunosuppressive genes, and tumor mutational burden (TMB). The difference of gene mutant frequency in high- and low-TPD52L2 groups was also analyzed. The results showed that TPD52L2 was over-expressed and predicted worse survival status in LUAD. We also found that TPD52L2 expression was positively associated with the infiltration levels of immunosuppressive cells, such as regulatory T cells (Tregs) and tumor-associated macrophages (TAMs), and negatively correlated with immune killer cells, such as CD8+ T and NK cells in pan-cancer, including LUAD. In addition, TPD52L2 expression was associated with immunosuppressive genes and TMB. High expression of TPD52L2 was with more mutant frequency of TP53. In summary, our results show that TPD52L2 is an oncogene and a potential prognostic biomarker in LUAD. High TPD52L2 expression is a possible indicator of immune infiltration and associated with tumor immunosuppressive status in LUAD.
Highlights
Lung cancer is one of the most common malignant tumors, and more than 80% of them are nonsmall-cell lung cancer (NSCLC)
The results revealed that Tumor protein D52-like 2 (TPD52L2) expression was significantly increased in 19 of 33 tumor types, including bladder urothelial carcinoma (BLCA), breast invasive carcinoma (BRCA), colon adenocarcinoma (COAD), cholangiocarcinoma (CHOL), glioblastoma multiforme (GBM), head-and-neck squamous cell carcinoma (HNSC), kidney renal clear cell carcinoma (KIRC), kidney renal papillary cell carcinoma (KIRP), brain lower grade glioma (LGG), liver hepatocellular carcinoma (LIHC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC), ovarian serous cystadenocarcinoma (OV), pancreatic adenocarcinoma (PAAD), rectum adenocarcinoma (READ), stomach adenocarcinoma (STAD), testicular germ cell tumor (TGCT), thymoma (THYM), and uterine carcinosarcoma (UCS), while it was only lowly expressed in esophageal carcinoma (ESCA), acute myeloid leukemia (LAML), pancreatic adenocarcinoma (PAAD), thyroid carcinoma (THCA), and uterine corpus endometrial carcinoma (UCEC) (Figure 1A)
Recent research shows that the expression levels of TPD52L2 were upregulated in prostate cancer tissues, andincreased TPD52L2 expression is associated with clinical progression and poor prognosis in patients with prostate cancer, suggesting that TPD52L2 may be a potential prognostic marker for patients with prostate cancer (Ren et al, 2017)
Summary
Lung cancer is one of the most common malignant tumors, and more than 80% of them are nonsmall-cell lung cancer (NSCLC). Lung adenocarcinoma (LUAD) is the most frequent subtype of NSCLC worldwide, and the morbidity of LUAD has surpassed lung squamous carcinoma in recent years (Ferlay et al, 2018; Cao et al, 2020). Target therapy and immunotherapy have improved the prognosis of LUAD patients, the five-year survival is still at a low level (Ferlay et al, 2019; Jurisic et al, 2020). It is vital to indicate how to develop further effective therapeutic strategies to improve the survival of LUAD patients. The tumor microenvironment (TME) refers to the environment where tumor cells originate and develop and is one of the main causes of malignant cancer occurrence and progression (Gajewski et al, 2013). Inflammatory cells make up a significant proportion of the overall tumor mass, and among them, macrophages, called tumor-associated macrophages (TAMs), which are abundant in the TME, could alleviate tumor immunity and promote tumor progression
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
