Effects of HMGA2 on the biological characteristics and stemness acquisition of gastric cancer cells

Background and study aims: The high mobility group A2 (HMGA2), a nonhistone nuclear binding protein, modulates transcription by altering the chromatin architecture of the target gene DNA in its specific AT-hooks region. HMGA2 overexpression has been observed in embryonic tissue and many malignant neoplasms. This study sought to verify whether HMGA2 plays a role in the biological functions of gastric cancer cells, such as cell proliferation, invasiveness, migration, and stem cell acquisition, and to provide some ideas for further research on the metastatic mechanism of gastric cancer.

Patients and methods: HMGA2's effects on the proliferation, invasiveness, and migration capabilities of gastric cancer cells were individually detected by BrdU, Transwell, and wound healing assays. Western blotting and immunofluorescence were used to evaluate whether HMGA2 could promote the acquisition of gastric cancer cells. Biostatistical analyses were performed using SPSS 17.0 for Windows.

Results: HMGA2 expression levels in gastric cancer cell lines were significantly higher than those in human immortalized gastric epithelial cell lines (p < 0.01). Gastric cancer cell proliferation was inhibited when HMGA2 was overexpressed (p < 0.05). The invasiveness and migration capabilities of gastric cancer cells with HMGA2 overexpression were enhanced more than those of the corresponding control groups (p < 0.05). HMGA2 overexpression promotes the stemness acquisition of stem cells from gastric cancer cells.

Conclusions: This study verified that the HMGA2 structural transcription factor promotes invasiveness, migration, and acquisition of gastric cancer cells. Furthermore, our findings provide significant insight for further research on the metastatic mechanism of gastric cancer.