ArticleHistology and histopathology2026
HNMT promotes the motility-associated structures of breast cancer cells through the PI3K/Akt signaling pathway to promote tumor progression.
Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundBreast cancer (BC) is a tumor type that severely threatens the health and lives of women worldwide. Cancer cell motility often leads to the distant metastasis of BC. Histamine N-methyltransferase (HNMT) has been reported to be associated with poor prognosis in patients with BC; however, its role in BC cell motility remains unclear. Therefore, this study aimed to investigate the role of HNMT in BC cell motility.
methodsMDA-MB-231 cells were injected into the mammary fat pads of female BALB/c nude mice to establish a BC orthotopic tumor model, and BC lung metastasis was evaluated via HE staining. To investigate the effects of HNMT on the malignant behavior of BC cells, HNMT was knocked down or overexpressed in MDA-MB-231 cells. Cell proliferation, migration and invasion were analyzed by using CCK-8, scratch and Transwell assays, respectively. Moreover, the expression of key genes and proteins was detected via RT-qPCR, Western blotting, immunofluorescence and immunohistochemistry; additionally, the formation of invasive pseudopodia was detected via phalloidin staining.
resultsHNMT expression was upregulated in BC. HNMT knockdown inhibited BC growth and lung metastasis
conclusionHNMT promoted BC cell invasion and metastasis through the activation of the PI3K/AKT signaling pathway, thereby promoting the malignant progression and lung tumor metastasis of BC. This study provides novel insights and potential therapeutic strategies for BC treatment.
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