Zhang Minqing, Du Yiping, Shang Jingmei, Zhang Dongqing, Dong Xiaoqing, Chen Hong
Department of Clinical Laboratory, Chengwu County People's Hospital, Chengwu Hospital Affiliated to Shandong First Medical University, Heze, Shandong 274200, P.R. China.
Department of Hematology, Qingdao Eighth People's Hospital, Qingdao, Shandong 266100, P.R. China.
Oncol Lett. 2021 Jan;21(1):39. doi: 10.3892/ol.2020.12300. Epub 2020 Nov 13.
Long non-coding RNA urothelial cancer associated 1 (UCA1) has been reported to act as a carcinogen in bladder cancer, while its role in diffuse large B-cell lymphoma (DLBCL) remains unclear. The present study was designed to explore the expression pattern and role of UCA1 in DLBCL. The expression pattern of UCA1 and microRNA (miR)-331-3p in DLBCL tissues and cell lines were detected by RT-qPCR. Dual luciferase reporter assay was performed to explore the relationship between UCA1 and miR-331-3p. Cell proliferation was explored by MTT assay. Cell migration and invasion abilities were assessed by Transwell assay. In the present study, it was revealed that the expression of UCA1 was significantly upregulated, while miR-331-3p was downregulated in DLBCL tissues and cell lines. Moreover, UCA1 was revealed to competitively bind with miR-331-3p in DLBCL. Functionally, knockdown of UCA1 was revealed to suppress cell proliferation, migration and invasion in DLBCL cells. Furthermore, upregulation of miR-331-3p prevented cell proliferation, migration and invasion in DLBC cells. In conclusion, the present findings firstly demonstrated that UCA1 silencing restrained DLBCL cell proliferation and metastases viability by suppressing miR-331-3p expression. It is suggested that UCA1 could be a possible medicinal target and biomarker for DLBCL.
长链非编码RNA尿路上皮癌相关1(UCA1)已被报道在膀胱癌中作为一种致癌因子发挥作用,而其在弥漫性大B细胞淋巴瘤(DLBCL)中的作用仍不清楚。本研究旨在探讨UCA1在DLBCL中的表达模式及作用。通过RT-qPCR检测DLBCL组织和细胞系中UCA1和微小RNA(miR)-331-3p的表达模式。进行双荧光素酶报告基因检测以探讨UCA1与miR-331-3p之间的关系。通过MTT检测探讨细胞增殖情况。通过Transwell检测评估细胞迁移和侵袭能力。在本研究中,结果显示在DLBCL组织和细胞系中UCA1的表达显著上调,而miR-331-3p的表达下调。此外,在DLBCL中UCA1被发现与miR-331-3p竞争性结合。在功能上,UCA1的敲低被发现可抑制DLBCL细胞的增殖、迁移和侵袭。此外,miR-331-3p的上调可阻止DLBC细胞的增殖、迁移和侵袭。总之,本研究结果首次证明UCA1沉默通过抑制miR-331-3p表达抑制DLBCL细胞增殖和转移能力。提示UCA1可能是DLBCL的一个潜在治疗靶点和生物标志物。