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Tumor Progression / Cell Line, Tumor / Breast Neoplasms · Research article (mechanistic)
Cancer Biology & Therapy · June 15, 2026
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STARD10, a lipid transport protein, was found to be upregulated in HER2+ breast cancer tissues and correlated with poor prognosis. Preclinical experiments in cell lines and mouse models demonstrated that STARD10 overexpression promotes proliferation, invasion, metastasis, and lipid droplet accumulation via the cAMP/PKA/CREB1 signaling axis.
Preclinical mechanistic study combining database analysis, in vitro cell assays, and in vivo mouse models. HER2+ breast cancer cell lines (SKBR3 and HCC1954) and mouse xenograft models; clinical cohort characteristics not specified. Intervention: STARD10 overexpression.
STARD10 expression was upregulated in HER2+ breast cancer tissues and significantly correlated with poor prognosis STARD10 overexpression enhanced HER2+ breast cancer cell proliferation, migration, invasion, and lipid droplets accumulation STARD10 overexpression markedly accelerated tumor growth and lung metastasis in vivo
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These findings identify STARD10 and the cAMP/PKA/CREB1 pathway as potential therapeutic targets in HER2+ breast cancer, particularly for patients with aggressive disease. However, clinical validation and therapeutic development are required before translation to practice.
Preclinical in vitro and mouse model evidence linking STARD10 to HER2+ breast cancer progression via lipid metabolism, without clinical efficacy data.
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These findings identify STARD10 and the cAMP/PKA/CREB1 pathway as potential therapeutic targets in HER2+ breast cancer, particularly for patients with aggressive disease. However, clinical validation and therapeutic development are required before translation to practice.
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Background. Although targeted therapies have improved clinical outcomes, HER2+ breast cancer remains a significant clinical challenge due to its aggressive behavior and unfavorable prognosis. Emerging evidence indicates that dysregulated lipid metabolism plays a critical role in tumorigenesis and metastasis, suggesting that targeting lipid metabolism may represent a promising therapeutic strategy. STARD10, a lipid transport protein, plays a pivotal role in regulating lipid metabolism. However, its function in mediating lipid metabolism and tumor progression in HER2+ breast cancer remains unclear.Methods. The expression level and prognostic relevance of STARD10 in HER2+ breast cancer were analyzed using public databases and clinical cohorts. CCK-8, EdU, colony formation, transwell, LD540, and Nile Red staining assays were performed in SKBR3 and HCC1954 cells. Subcutaneous implantation and tail vein injection were performed to evaluate the effects of STARD10 overexpression on tumor growth and lung metastasis in vivo. The mechanism was validated by RNA-seq and Western blotting.Results. STARD10 expression was upregulated in HER2+ breast cancer tissues and was significantly correlated with poor prognosis. Functionally, STARD10 overexpression enhanced HER2+ breast cancer cell proliferation, migration, invasion, and lipid droplets accumulation. Moreover, STARD10 overexpression markedly accelerated tumor growth and lung metastasis in vivo. Mechanistically, STARD10 was found to drive malignant phenotypes via activation of the cAMP/PKA/CREB1 signaling axis.Conclusion. STARD10 promotes malignant progression of HER2+ breast cancer and lipid droplets accumulation by activating the cAMP/PKA/CREB1 pathway. These findings suggest that STARD10 and the cAMP/PKA/CREB1 signaling axis as potential therapeutic targets for the treatment and prevention of HER2+ breast cancer.
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