Pang Xunlei, Wang Yanhong, Miao Bei, Fei Sujuan, Chen Weichang
Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215008, P.R. China.
Department of Gastroenterology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221004, P.R. China.
Oncol Lett. 2021 Mar;21(3):196. doi: 10.3892/ol.2021.12457. Epub 2021 Jan 11.
Colorectal cancer (CRC) is the third most common malignant disease in adults. ADP ribosylation factor-like GTPase 2 (ARL2) is crucial for controlling the dynamics of microtubules and mitochondrial functions. However, the biological function of ARL2 in CRC remains unclear. The present study was performed to identify the expression level and functional role of ARL2 in CRC. A total of 19 CRC and 3 normal healthy colorectal tissues were collected. Furthermore, ARL2 expression was analyzed in healthy colorectal and CRC tissues by immunohistochemistry (IHC). ARL2 overexpression and knockdown was achieved using lentiviral vectors and plasmid transfection in HCT8 and HCT116 cells. The protein and mRNA expression levels of ARL2 and AXL were analyzed using western blot and reverse transcription-quantitative PCR in ARL2 knockdown and ARL2 overexpressing HCT8 and HCT116 cells. Cell Counting Kit-8, colony formation, wound healing, and Matrigel assays were used to investigate the biological functions of ARL2. Taken together, ARL2 protein expression level was upregulated in CRC tissues. Furthermore, ARL2 overexpression decreased proliferation and weakened the colony-formation abilities of the CRC cells, as well as their migratory and invasive abilities. ARL2 interference enhanced proliferation and colony-formation rates of the CRC cells, as well as their migratory and invasive abilities. ARL2 regulated CRC proliferation and tumorigenicity and was negatively associated with AXL. The results of the present study suggested that the proliferation, migration and tumorigenicity of the CRC cells could be inhibited by ARL2 overexpression. The latter may be used as a predicted and potential therapeutic target for CRC.
结直肠癌（CRC）是成年人中第三大常见恶性疾病。ADP核糖基化因子样GTP酶2（ARL2）对于控制微管动力学和线粒体功能至关重要。然而，ARL2在结直肠癌中的生物学功能仍不清楚。本研究旨在确定ARL2在结直肠癌中的表达水平和功能作用。总共收集了19份结直肠癌组织和3份正常健康的结直肠组织。此外，通过免疫组织化学（IHC）分析了健康结直肠组织和结直肠癌组织中ARL2的表达。在HCT8和HCT116细胞中使用慢病毒载体和质粒转染实现了ARL2的过表达和敲低。在ARL2敲低和过表达的HCT8和HCT116细胞中，使用蛋白质印迹法和逆转录定量PCR分析了ARL2和AXL的蛋白质和mRNA表达水平。使用细胞计数试剂盒-8、集落形成、伤口愈合和基质胶实验来研究ARL2的生物学功能。综上所述，结直肠癌组织中ARL2蛋白表达水平上调。此外，ARL2过表达降低了结直肠癌细胞的增殖能力，削弱了其集落形成能力以及迁移和侵袭能力。ARL2干扰增强了结直肠癌细胞的增殖和集落形成率，以及它们的迁移和侵袭能力。ARL2调节结直肠癌的增殖和致瘤性，并且与AXL呈负相关。本研究结果表明，ARL2过表达可抑制结直肠癌细胞的增殖、迁移和致瘤性。后者可能作为结直肠癌的一个预测性和潜在治疗靶点。
