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STAT1 accelerates cutaneous melanoma progression through TUBB4A expression regulation
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DOI：10.3892/mmr.2026.13828.png)
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Abstract
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The present research explored the contributions of signal transducer and activator of transcription 1 (STAT1) and tubulin beta 4A (TUBB4A) in melanoma pathogenesis, focusing on their roles in modulating cellular proliferation, motility and apoptotic pathways. The goal of the study was to establish foundational evidence of the role of these proteins in melanoma for the development of precision therapeutic interventions. Gene silencing approaches were utilized to suppress STAT1 expression, while TUBB4A overexpression was achieved both in vitro and in a murine xenograft model. Cellular proliferation was evaluated via Cell Counting Kit-8 and colony formation assay, whereas migration capacity was assessed using Transwell migration assays. Apoptotic activity was quantified by flow cytometry using Annexin V-FITC and PI staining. Western blot analysis was performed to measure the protein expression levels of STAT1 and TUBB4A. STAT1 downregulation led to impaired proliferation and motility in A375 and RPMI-7951 melanoma cell lines, concomitant with increased apoptotic rates. These phenotypic changes were partially reversed following TUBB4A overexpression. In vivo experiments demonstrated significantly smaller tumor volumes in STAT1 knockdown xenografts, although TUBB4A overexpression partially restored neoplastic growth. STAT1 drove melanoma progression by upregulating TUBB4A, which acted as a downstream signaling mediator. The ability of TUBB4A to counteract STAT1 inhibition effects suggested that targeting this regulatory axis represents a potential therapeutic strategy. The findings of the present study contributed novel mechanistic insights that may facilitate the development of innovative melanoma treatment modalities.
Keywords:
STAT1
cutaneous melanoma
TUBB4A
apoptosis
migration
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