Cucurbitacin B Inhibits the Malignancy of Esophageal Carcinoma through the KIF20A/JAK/STAT3 Signaling Pathway.

The American journal of Chinese medicine Pub Date : 2024-01-01 Epub Date: 2024-01-30 DOI:10.1142/S0192415X24500125
Chao Liu, Jian Ji, Chenglin Li
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Abstract

This study intends to explore the effects of Cucurbitacin B (CuB) and KIF20A on esophageal carcinoma (ESCA). Data were downloaded from the Cancer Genome Atlas (TCGA) database. The expression properties of KIF20A have been confirmed by GEPIA and ualcan from TCGA. The expression of KIF20A was determined using western blotting in ECA109 and KYSE150 cells after transfection with KIF20A, KIF20A siRNA, or numerical control siRNA (si-NC). Then, different concentrations of CuB were used to treat ECA109 and KYSE150 cells. CCK-8 and colony formation assays were used to measure cell viability, and a Transwell assay was utilized to assess cell migration and invasion ability. N-cadherin, E-cadherin, snail, p-Janus kinase 2 (JAK2), JAK2, p-signal transducer and activator of transcription 3 (STAT3), and STAT3 expression levels were evaluated using western blot. KIF20A was higher expressed in ESCA than in normal cells, and its overexpression was associated with squamous cell carcinoma, TNM stage, and lymph nodal metastasis of ESCA patients. In ECA109 and KYSE150 cells, increased KIF20A facilitated cell proliferation, migration, and invasion, whereas the knockdown of KIF20A can reverse these effects with N-cadherin. Snail expression diminished and E-cadherin increased. Similarly, CuB treatment could inhibit cell proliferation, migration, and invasion concentration dependently. Furthermore, KIF20A accelerated the expression of p-JAK2 and p-STAT3, while the application of CuB inhibited KIF20A expression and attenuated the activation of the JAK/STAT3 pathway. These findings revealed that CuB could inhibit the growth, migration, and invasion of ESCA through downregulating the KIF20A/JAK/STAT3 signaling pathway, and CuB could serve as an essential medicine for therapeutic intervention.

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葫芦素 B 通过 KIF20A/JAK/STAT3 信号通路抑制食管癌的恶性发展
本研究旨在探讨葫芦素B(CuB)和KIF20A对食管癌(ESCA)的影响。数据下载自癌症基因组图谱(TCGA)数据库。KIF20A 的表达特性已由 TCGA 的 GEPIA 和 ualcan 证实。在转染 KIF20A、KIF20A siRNA 或数值对照 siRNA(si-NC)后的 ECA109 和 KYSE150 细胞中,用 Western 印迹法测定 KIF20A 的表达。然后用不同浓度的 CuB 处理 ECA109 和 KYSE150 细胞。CCK-8和集落形成试验用于测定细胞活力,Transwell试验用于评估细胞迁移和侵袭能力。用 Western 印迹法评估了 N-cadherin、E-cadherin、蜗牛、p-Janus 激酶 2(JAK2)、JAK2、p-信号转导和激活转录 3(STAT3)以及 STAT3 的表达水平。KIF20A在ESCA中的表达高于正常细胞,其过表达与ESCA患者的鳞状细胞癌、TNM分期和淋巴结转移有关。在 ECA109 和 KYSE150 细胞中,KIF20A 的增加促进了细胞的增殖、迁移和侵袭,而 KIF20A 的敲除可与 N-cadherin一起逆转这些效应。蜗牛表达减少,E-cadherin 增加。同样,CuB 处理可抑制细胞增殖、迁移和侵袭的浓度依赖性。此外,KIF20A 可加速 p-JAK2 和 p-STAT3 的表达,而 CuB 可抑制 KIF20A 的表达并减轻 JAK/STAT3 通路的激活。这些研究结果表明,CuB可通过下调KIF20A/JAK/STAT3信号通路抑制ESCA的生长、迁移和侵袭,CuB可作为一种重要的治疗干预药物。
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