探讨泛酸激酶1（PANK1）在肾透明细胞癌（KIRC）组织中的表达，分析其与临床病理特征和预后的相关性，探讨其对KIRC细胞侵袭、迁移和凋亡的影响。采用 UALCAN 和 LinkedOmics 分析 KIRC 组织中的 PANK1 表达及其与临床特征的相关性。在 KIRC（Caki-1 和 786-O）和非癌肾细胞（HK-2 和 RPTEC）之间进行比较分析。用PANK1激活颗粒转染，然后进行伤口愈合、Transwell实验、Annexin V-异硫氰酸荧光素/碘化丙啶（Annexin V-FITC/PI）染色、定量逆转录聚合酶链反应（qRT-PCR）和Western blotting与正常组织和非癌细胞相比，PANK1 在 KIRC 组织和细胞中表达下调。相关分析将 PANK1 表达与 KIRC 的临床病理特征联系起来，高 PANK1 表达与良好的结果相关。 PANK1 高表达与 E-钙粘蛋白 (CDH1)、紧密连接蛋白 1 (TJP1)、Fas 细胞表面死亡受体 (FAS)、caspase-8 (CASP8) 和 CASP9 呈正相关，而与波形蛋白 (VIM) 呈负相关、 蜗牛家族转录抑制因子 1 (SNAIL1)、扭曲家族 BHLH 转录因子 1 (TWIST1) 和 TWIST2。 PANK1过表达使KIRC细胞CDH1、TJP1、FAS、CASP8和CASP9上调，同时下调SNAIL1、VIM、TWIST1和TWIST2，抑制侵袭和迁移，促进KIRC细胞凋亡。KIRC组织中PANK1下调与临床病理特征和预后相关。它的过表达调节上皮间质转化 (EMT) 相关基因，抑制侵袭，促进 KIRC 细胞凋亡，突出其在疾病进展和治疗潜力中的作用。© 2024。作者。

To investigate pantothenate kinases 1 (PANK1) expression in kidney renal clear cell carcinoma (KIRC) tissues, analyze its correlation with clinicopathological features and prognosis, and explore its impact on invasion, migration, and apoptosis in KIRC cells.GEPIA (gene expression profiling interactive analysis), UALCAN and LinkedOmics, were employed to analyze PANK1 expression in KIRC tissues and its correlation with clinical characteristics. Comparative analyses were performed between KIRC (Caki-1 and 786-O) and noncancerous renal cells (HK-2 and RPTEC). Transfection with PANK1 activation particles was conducted, followed by Wound healing, Transwell assay, Annexin V-fluorescein isothiocyanate/propidium iodide (Annexin V-FITC/PI) staining, quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and Western blotting.PANK1 was down-regulated in KIRC tissues and cells compared to normal tissues and noncancerous cells. Correlation analyses linked PANK1 expression with clinicopathological features in KIRC, with high PANK1 expression associated with a favorable outcome. High PANK1 expression correlated positively with E-cadherin (CDH1), tight junction protein 1 (TJP1), Fas cell surface death receptor (FAS), caspase-8 (CASP8), and CASP9, while showing a negative correlation with vimentin (VIM), snail family transcriptional repressor 1 (SNAIL1), twist family BHLH transcription factor 1 (TWIST1), and TWIST2. PANK1 overexpression increased CDH1, TJP1, FAS, CASP8, and CASP9 while downregulating SNAIL1, VIM, TWIST1, and TWIST2, inhibiting invasion and migration, and promoting apoptosis in KIRC cells.PANK1 down-regulation in KIRC tissues correlated with clinicopathological features and prognosis. Its overexpression modulated epithelial-mesenchymal transition (EMT)-related gene, inhibited invasion, promoted apoptosis in KIRC cells, highlighting its role in disease progression and therapeutic potential.© 2024. The Author(s).