ETS-1 in tumor immunology: implications for novel anti-cancer strategies

Abstract

ETS-1, a key member of the Erythroblast Transformation-Specific (ETS) transcription factor family, plays an important role in cell biology and medical research due to its wide expression profile and strong transcriptional regulation ability. It regulates fundamental biological processes, including cell proliferation, differentiation, and apoptosis, and is involved in tumorigenesis and metastasis, promoting malignant behaviors such as angiogenesis, matrix degradation, and cell migration. Given the association between ETS-1 overexpression and the aggressive characteristics of multiple malignancies, it represents a promising therapeutic target in cancer treatment. This study aims to systematically analyze the role of ETS-1 within the tumor immune microenvironment, elucidating its mechanisms in cancer initiation, progression, and metastasis. It also investigates the differential expression of ETS-1 across tumor tissues and adjacent normal tissues, exploring its potential as a molecular marker for tumor diagnosis and prognosis.

Keywords: ETS family; ETS-1; biological functions; immune microenvironment; immunotherapy targets; tumor immunology.

Figure 1

ETS protein structure. The ETS1 Pointed domain, the acidic transactivation domain, the autoinhibitory domains, and the Ets DNA binding domain, are indicated. Also shown is the conserved MAP kinase phosphorylation site (T38) found at the N-terminus of ETS1 protein.

Figure 2

The regulatory effect of ETS-1 related signaling pathway on tumor biological processes. This figure shows the role of ETS-1 in cell proliferation, cell migration, immune escape and angiogenesis through the three main signaling pathways of MAPK/ERK, PI3K/Akt and TGF-β.

Figure 3

The expression of ETS-1 in different tumors. The map contains the role of ETS1 in breast cancer, gastric cancer, colorectal cancer, prostate cancer, kidney cancer, liver cancer, cervical cancer, pancreatic cancer and nasopharyngeal carcinoma.