Xie Tingting, Guo Jianian, Wang Wei
Department of Gastroenterology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Department of Thoracic Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No.250 Changgang East Road, Haizhu District, Guangzhou, 510260, China.
Biochem Genet. 2025 Apr;63(2):1719-1733. doi: 10.1007/s10528-024-10786-6. Epub 2024 Apr 12.
This study aimed to determine the role of the long noncoding RNA (lncRNA) gall bladder cancer-associated suppressor of pyruvate carboxylase (SOD2-1) in the progression of colorectal cancer (CRC). A total of 23 pairs of specimens, including CRC tissues and adjacent normal tissues, were collected, and the expression of lncRNA SOD2-1 (lnc-SOD2-1) was measured. lnc-SOD2-1 function was examined using HCT15 and HCT116 cells. A lnc-SOD2-1 overexpression vector was designed and transfected into both cell lines. MTS and colony formation assays were used to determine cell viability. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assays were performed to measure apoptosis. Cell migration and invasion were evaluated using the Transwell assay. Migration and invasion markers were validated using quantitative reverse transcription-polymerase chain reaction and western blot analysis. The results indicated that the expression of lnc-SOD2-1 was downregulated in CRC tissues. lnc-SOD2-1 overexpression evidently decreased cell viability and led to the formation of fewer cell colonies. lnc-SOD2-1 overexpression induced ~ twofold higher apoptosis than the control group. lnc-SOD2-1 overexpression reduced the proportion of migratory and invasive cells to 50% and 75% of the control group, respectively. lnc-SOD2-1 overexpression significantly decreased the expression of matrix metalloproteinase-2 and -9. In conclusion, lnc-SOD2-1 may act as a tumor suppressor that inhibits the proliferation, migration, and invasion of CRC cells and induces their apoptosis.
本研究旨在确定长链非编码RNA(lncRNA)胆囊癌相关丙酮酸羧化酶抑制因子(SOD2-1)在结直肠癌(CRC)进展中的作用。共收集了23对标本,包括CRC组织和相邻正常组织,并检测了lncRNA SOD2-1(lnc-SOD2-1)的表达。使用HCT15和HCT116细胞检测lnc-SOD2-1的功能。设计了lnc-SOD2-1过表达载体并转染到这两种细胞系中。采用MTS和集落形成试验来确定细胞活力。进行流式细胞术和末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记试验以检测细胞凋亡。使用Transwell试验评估细胞迁移和侵袭能力。使用定量逆转录-聚合酶链反应和蛋白质免疫印迹分析验证迁移和侵袭标志物。结果表明,lnc-SOD2-1在CRC组织中的表达下调。lnc-SOD2-1过表达明显降低细胞活力并导致形成的细胞集落减少。lnc-SOD2-1过表达诱导的细胞凋亡比对照组高约两倍。lnc-SOD2-1过表达分别将迁移和侵袭细胞的比例降低至对照组的50%和75%。lnc-SOD2-1过表达显著降低基质金属蛋白酶-2和-9的表达。总之,lnc-SOD2-1可能作为一种肿瘤抑制因子,抑制CRC细胞的增殖、迁移和侵袭并诱导其凋亡。