黑色素瘤是癌症死亡的主要原因之一。驱动蛋白家族成员22（KIF22）对于黑色素瘤细胞的侵袭至关重要，但KIF22在黑色素瘤增殖和糖酵解中的作用和机制仍不清楚。黑色素瘤组织中KIF22的表达以及KIF22高表达与黑色素瘤总生存率的关系使用 Tnmplot 数据库对黑色素瘤患者进行分析。通过蛋白质印迹检查黑色素瘤细胞中的 KIF22 表达。然后，沉默KIF22并采用CCK-8测定、EDU染色和流式细胞术分析来评估细胞增殖和凋亡。此外，通过检测细胞外酸化率（ECAR）和耗氧率（OCR）来反映黑色素瘤细胞的糖酵解代谢情况。通过蛋白质印迹测试与凋亡、糖酵解和EGFR/STAT3信号传导相关的蛋白的表达。随后，用EGF或Colivelin处理黑色素瘤细胞，进一步阐明KIF22对EGFR/STAT3信号传导的调节作用。黑色素瘤组织和细胞中KIF22表达显着上调，KIF22高表达与不良预后相关。此外，KIF22 不足会抑制黑色素瘤细胞的增殖并加速其凋亡。此外，KIF22 消耗导致糖酵解减少，ECAR 降低和 OCR 增加证明，同时 HK2、PKM2 和 LDHA 表达下调。重要的是，KIF22 缺失对黑色素瘤进展的影响在 EGF 或 Colivelin 治疗后部分减弱。总的来说，KIF22 敲除抑制了增殖和糖酵解，并通过灭活 EGFR/STAT3 信号传导促进黑色素瘤细胞凋亡。版权所有 © 2023 HCFMUSP。由 Elsevier España 出版，S.L.U.版权所有。

Melanoma is one of the leading causes of cancer death. Kinesin Family member 22 (KIF22) is essential for the invasion of melanoma cells, but the role and mechanism of KIF22 in the proliferation and glycolysis in melanoma remains unknown.KIF22 expression in melanoma tissues and the relationship between KIF22 high expression and overall survival rate in patients with melanoma were analyzed using the Tnmplot database. KIF22 expression in melanoma cells was examined by western blot. Then, KIF22 was silenced and CCK-8 assay, EDU staining and flow cytometry analysis were adopted for assessing cell proliferation and apoptosis. In addition, the glycolysis metabolism of melanoma cells was reflected by detecting Extracellular Acidification Rates (ECAR) and Oxygen Consumption Rates (OCR). The expression of proteins related to apoptosis, glycolysis and EGFR/STAT3 signaling was tested by western blot. Subsequently, melanoma cells were treated with EGF or Colivelin to further elucidate the regulatory effect of KIF22 on EGFR/STAT3 signaling.KIF22 expression was notably upregulated in melanoma tissues and cells, and KIF22 high expression was associated with a poor prognosis. Moreover, KIF22 insufficiency suppressed proliferation and accelerated apoptosis of melanoma cells. Additionally, glycolysis was reduced by KIF22 depletion, evidenced by the decreased ECAR and increased OCR, accompanied by the downregulated expression of HK2, PKM2 and LDHA. Importantly, the impacts of KIF22 depletion on the progression of melanoma were partially attenuated after EGF or Colivelin treatment.Collectively, KIF22 knockdown suppressed the proliferation and glycolysis and facilitated the apoptosis of melanoma cells by inactivating EGFR/STAT3 signaling.Copyright © 2023 HCFMUSP. Published by Elsevier España, S.L.U. All rights reserved.