Abstract
BackgroundAnti‐silencing function 1 (ASF1) is a conserved histone H3–H4 chaperone protein. ASF1B, a paralog of ASF1, acts by promoting cell proliferation and influencing cell cycle progression. Although there is some evidence demonstrating that ASF1B plays a key role in the development, progression, and prognosis of certain cancers, there are no pan‐cancer analyses of ASF1B.MethodsWe used a range of bioinformatics approaches to investigate the predictive role of ASF1B, including its correlation with prognosis, tumor mutational burden (TMB), microsatellite instability (MSI), tumor microenvironment (TME), and immune cell infiltration, in diverse cancer types.ResultsWe found that ASF1B was highly expressed in 22 cancers and was negatively correlated with the prognosis of multiple major cancer types. Furthermore, ASF1B expression was correlated with TMB in 21 cancers and with MSI in 7 cancers. We found that ASF1B was coexpressed with genes encoding immune activators, immune suppressors, major histocompatibility complexes, chemokines, and chemokine receptors. We further found that the role of ASF1B in the infiltration of different types of immune cells varied across tumor types. ASF1B may potentially affect several key immune‐related pathways, such as those involved in antigen processing and presentation, natural killer cell‐mediated cytotoxicity, and autoimmune thyroid disease.ConclusionsOur findings show that ASF1B may serve as a prognostic marker and potential immunotherapeutic target for several malignancies due to its role in tumorigenesis and immune infiltration.
Highlights
Cancer is caused by a complicated series of events that leads to uncontrolled cell growth and enables cells to evade natural cell death mechanisms, resulting in malignancy and high lethality.[1]
The results indicated that the expression of ASF1B was significantly increased in most cancer types, including bladder cancer (BLCA), brain and central nervous system (CNS) cancer, breast cancer (BRCA), cervical cancer (CESC), colorectal cancer (COAD), esophageal cancer (ESCA), gastric cancer, head, and neck cancer (HNSC), kidney cancer, liver cancer (LIHC), lung cancer, lymphoma, myeloma, ovarian cancer (OV), pancreatic cancer (PAAD), and sarcoma (SARC) (Figure 1A)
We found that ASF1B expression was significantly elevated in 20 of the 33 cancer types, including BLCA, BRCA, CESC, bile duct cancer (CHOL), COAD, ESCA, glioblastoma (GBM), HNSC, kidney chromophobe (KICH), kidney clear cell carcinoma (KIRC), kidney papillary cell carcinoma (KIRP), LIHC, lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC), prostate cancer (PRAD), rectal cancer (READ), SARC, stomach cancer (STAD), thyroid cancer (THCA), and endometrioid cancer (UCEC)
Summary
Cancer is caused by a complicated series of events that leads to uncontrolled cell growth and enables cells to evade natural cell death mechanisms, resulting in malignancy and high lethality.[1]. The number of approved immunotherapy drugs, which kill cancer cells by activating and boosting the body's own immune system, continues to rise.[3] With the development and refinement of pan-cancer gene expression databases, it is easier than ever to identify new immunotherapeutic targets, assess their clinical value, and determine their associated signaling pathways. This work offers a basis for understanding the mechanism of action of ASF1B in various cancers and provides a rationale for targeting ASF1B with immunotherapies
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