Abstract
Homeobox C10 (HOXC10) has been reported to participate in various cancers. However, the involvement of HOXC10 in melanoma is still unknown. Here, we attempted to determine whether HOXC10 can affect the development of melanoma. We separated melanoma tissues and the matched tumor-adjacent normal tissues from melanoma patients, and examined HOXC10 expression in the melanoma cells and tissues. Comparing with the tumor-adjacent normal tissues, HOXC10 was up-regulated in melanoma tissues. Melanoma cells also displayed an up-regulation of HOXC10. Moreover, HOXC10 inhibition suppressed cell proliferation, clone formation and promoted apoptosis of melanoma cells. Knockdown of HOXC10 also retarded migration, invasion and epithelial–mesenchymal transition (EMT) in melanoma cells. Additionally, HOXC10 accelerated Slug expression by interacting with Slug, and activating the promoter of Slug. Slug activated the YAP/TAZ signaling pathway, which was reversed by HOXC10 silencing. The in vitro assays demonstrated that inhibition of HOXC10 significantly repressed tumor growth and lung metastasis of melanoma in mice by inhibiting Slug and YAP/TAZ signaling pathway. In conclusion, this work demonstrated that HOXC10 promoted growth and migration of melanoma by regulating Slug to activate the YAP/TAZ signaling pathway. Therefore, this study suggests that inhibition of HOXC10 has therapeutic potential in melanoma.
Highlights
Melanoma is an malignant epithelial tumor that originates from the melanocytes of neural crest, that is, a malignant change in pigmented nevus [1]
We initially compared Homeobox C10 (HOXC10) expression between melanoma tissues and tumor-adjacent normal tissues of patients with melanoma
HOXC10 is a target of miR-129-5p, and miR-129-5p inhibits gastric cancer development by regulating HOXC10/Cyclin D1 axis [22]
Summary
Melanoma is an malignant epithelial tumor that originates from the melanocytes of neural crest, that is, a malignant change in pigmented nevus [1]. Melanoma is a highly malignant, most aggressive and lethal tumor among human skin cancer. It originates from the imbalance of melanocyte proliferation, which accounts for more than 80% of skin cancerrelated deaths [2]. The latest research conclusions point out that long-term exposure to strong sunlight, genetic mutations and environmental factors may cause the malignant transformation of nevus and pigmented spots into melanoma [3, 4]. Scholars have conducted a large number of researches and clinical trials to explore the potential molecular pathogenesis and treatment strategies of melanoma. It has been proved that various pathways are associated with the occurrence of melanoma, such as MAPK, PI3K/Akt and YAP/TAZ pathways [5,6,7,8]
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