Exploration of targeted anti-tumor therapy · 2026
Mechanistic study of antisense long non-coding RNA STEAP3-AS1 in breast cancer.
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Sun Jinquan, Cui Jiayong, Qiu Tianlei, Shen Guoshuang
Аннотация
AIM: This study aims to investigate the expression and function of antisense long non-coding RNA (lncRNA) STEAP3-AS1 in breast cancer (BC). Additionally, it explores STEAP3's regulatory relationship with STEAP3-AS1 and potential signaling pathways to provide a theoretical foundation for identifying novel therapeutic targets.
METHODS: Database prediction and collection of tissue samples were employed alongside a cell proliferation assay and Transwell migration and invasion assay to examine STEAP3-AS1 expression levels in BC tissues and cell lines, as well as its impact on cellular functions. Statistical analyses were performed, including two-tailed Student's t-test, Mann-Whitney U test and analysis of variance (ANOVA).
RESULTS: Both database and 9 paired clinical tissue sample results demonstrate that STEAP3-AS1 expression was significantly downregulated in BC compared with normal breast tissues (P < 0.05). Compared with the estrogen receptor/progesterone receptor (ERPR)-negative (-)/human epidermal growth factor receptor-2 (Her2)-positive (+) subtype, the ERPR(+)/Her2(-) and ERPR(-)/Her2(-) subtypes exhibited a significantly lower expression level of STEAP3-AS1 (P < 0.05). Overexpression of STEAP3-AS1 markedly suppressed the proliferation, migration, and invasion capabilities of MDA-MB-231 and MCF-7 cells compared with negative controls (P < 0.05). Furthermore, STEAP3-AS1 exhibited a positive synergistic effect with its sense strand STEAP3, inhibiting BC cell migration and invasion.
CONCLUSIONS: This study is the first to demonstrate the tumor-suppressive role of STEAP3-AS1 in BC. These findings provide novel insights into the mechanisms underlying BC progression and offer critical theoretical support for the development of new therapeutic strategies.
METHODS: Database prediction and collection of tissue samples were employed alongside a cell proliferation assay and Transwell migration and invasion assay to examine STEAP3-AS1 expression levels in BC tissues and cell lines, as well as its impact on cellular functions. Statistical analyses were performed, including two-tailed Student's t-test, Mann-Whitney U test and analysis of variance (ANOVA).
RESULTS: Both database and 9 paired clinical tissue sample results demonstrate that STEAP3-AS1 expression was significantly downregulated in BC compared with normal breast tissues (P < 0.05). Compared with the estrogen receptor/progesterone receptor (ERPR)-negative (-)/human epidermal growth factor receptor-2 (Her2)-positive (+) subtype, the ERPR(+)/Her2(-) and ERPR(-)/Her2(-) subtypes exhibited a significantly lower expression level of STEAP3-AS1 (P < 0.05). Overexpression of STEAP3-AS1 markedly suppressed the proliferation, migration, and invasion capabilities of MDA-MB-231 and MCF-7 cells compared with negative controls (P < 0.05). Furthermore, STEAP3-AS1 exhibited a positive synergistic effect with its sense strand STEAP3, inhibiting BC cell migration and invasion.
CONCLUSIONS: This study is the first to demonstrate the tumor-suppressive role of STEAP3-AS1 in BC. These findings provide novel insights into the mechanisms underlying BC progression and offer critical theoretical support for the development of new therapeutic strategies.