Colon adenocarcinoma is a frequent malignancy among all colon cancer types. Long non-coding RNAs (lncRNAs) are involved in the progression of colon adenocarcinoma. This study aimed to uncover the molecular mechanism of VPS9D1-AS1 in regulating colon adenocarcinoma development. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) revealed that VPS9D1-AS1 expression was markedly upregulated in colon adenocarcinoma tissues and cell lines. Cell functional experiments showed that knockdown of VPS9D1-AS1 repressed the growth and invasion of colon adenocarcinoma cells but upregulated cell apoptosis. In addition, we confirmed the interaction of VPS9D1-AS1-miR-1301-3p-CLDN1 using a luciferase assay. Downregulation of miR-1301-3p promoted the progression of colon adenocarcinoma cells. In conclusion, VPS9D1-AS1 facilitated cell growth and suppressed apoptosis of colon adenocarcinoma cells by sponging miR-1301-3p and upregulating CLDN1, which may be effective therapeutic strategies for patients with colon adenocarcinoma.

结肠腺癌是所有结肠癌类型中常见的恶性肿瘤。长链非编码 RNA (lncRNA) 与结肠腺癌的进展有关。本研究旨在揭示VPS9D1-AS1调控结肠腺癌发展的分子机制。定量逆转录聚合酶链反应 (RT-qPCR) 显示 VPS9D1-AS1 表达在结肠腺癌组织和细胞系中显着上调。细胞功能实验表明，敲低 VPS9D1-AS1 可抑制结肠腺癌细胞的生长和侵袭，但上调细胞凋亡。此外，我们使用荧光素酶测定证实了 VPS9D1-AS1-miR-1301-3p-CLDN1 的相互作用。miR-1301-3p的下调促进了结肠腺癌细胞的进展。综上所述，