Abstract
Objective To explore the relationship between CTCFL and DPPA2 and validate the positive role of CTCFL/DPPA2 in cell malignant behaviors in gastric cancer. Methods We predicted gastric cancer-related transcription factors and corresponding target mRNAs through bioinformatics. Levels of CTCFL and DPPA2 were assessed via qRT-PCR and western blot. In vitro experiments were utilized to assay the cell biological behaviors. CHIP was utilized for the assessment of the targeted relationship between CTCFL and DPPA2. Results CTCFL and DPPA2 were both highly expressed in gastric cancer cells, and high CTCFLL and DPPA2 could promote cell malignant behaviors. CHIP validated that DPPA2 was a target of CTCFL. In addition, high DPPA2 rescued the repressive impact of CTCFL silencing on the cell proliferation, migration, and invasion in gastric cancer. Conclusion The transcription factor CTCFL fosters cell proliferative, migratory, and invasive properties via activating DPPA2 in gastric cancer.
Highlights
Gastric cancer is a gastrointestinal malignancy responsible for mortality worldwide [1]
CTCFL (BORIS) is a pivotal DNA binding protein involved in tumor regulation, and it serves as a vital immunotherapeutic target [15, 16]
Pearson correlation analysis was conducted and found that there was a positive correlation between CTCFL and DPPA2 (Figure 1(e))
Summary
Gastric cancer is a gastrointestinal malignancy responsible for mortality worldwide [1]. Great advance has been achieved towards cancer treatment, whereas it is still a big challenge for gastric cancer treatment that metastasis occurs after the disease is radically cured [2]. It is necessary to perform in-depth research on the molecular mechanism underlying the migration and invasion of gastric cancer cells, as well as premise of cancer metastasis, so as to provide potential therapeutic strategies. CTCFL is a homology of CTCF harboring a nearly identical 11-zinc finger region [5]. These two proteins have similar binding specificity to DNA sequences due to the difference in the sequences on the amino and carboxyl terminals, but the protein functions are different [5]. In the current public literatures, CTCFL can mediate the onset and progression of varying cancers, such as liver cancer and neuroblastoma [6, 7], yet no relevant efforts have been made in gastric cancer
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