Gastric cancer (GC) is one of the leading cancers worldwide, which was estimated to affect 1,089,103 people and killed 768,793 in 2020 [1]. Gastric cancer patients are often diagnosed with advanced-stage malignancy at the time of the first admission, and some patients even have distant metastasis, which makes clinical treatment difficult. Although the survival rate of patients with different stages of gastric cancer showed different survival outcomes, the overall 5-year relative survival of patients with GC during 2017–2021 was 42.9 % [2]. It can be seen that there is still much room for improvement in the treatment of gastric cancer, while the elucidation of the molecular mechanism behind the progression of GC metastasis is very important.

As the key biological event in GC metastasis, EMT (epithelial-mesenchymal transition) is the pivotal process. EMT refers to the transformation of epithelium-like cells to mesenchyme-like cells. After this process, the original quiescent tumor cells become motile, which eventually contributes to tumor metastasis. The original cells, which show more properties of epithelium, could express specific markers like E-cadherin. The newly-produced mesenchymal-like cells could express biomarkers like N-cadherin, Vimentin, β-catenin, and α-SMA [3]. They can all be termed EMT-related proteins, indicating tumor progression and invasiveness.

Special AT-rich DNA-binding protein 1 (SATB1) is a transcription factor that plays significant roles in multiple cellular events. Physiologically, SATB1 is a chromatin organizer that specifically binds to AT-rich motifs in DNA and folds chromatin into loops to regulate the expression of a large set of genes [4]. Our previous meta-analysis study found that abnormal overexpression of SATB1 in gastrointestinal tumor tissue implies deeper tumor invasion depth and is more prone to lymph node and distant metastasis [5]. Recently, many studies found that SATB1 could regulate EMT to promote prostate cancer and breast cancer metastasis [6], [7]. To investigate the role of EMT in the molecular mechanism of GC metastasis related to SATB1, we designed the following studies.