Abstract：
TPT1 Antisense RNA 1 (TPT1-AS1) is a recently identified tumor oncogenic long non-coding RNA (lncRNA) in ovarian cancer and cervical cancer. This study was carried out to study the role of lncRNA TPT1-AS1 in hepatocellular carcinoma (HCC). Samples of HCC and non-tumor tissues derived from 62 HCC patients were subjected to RNA isolation and reverse transcription quantitative polymerase chain reaction to detect the differential expression of TPT1-AS1 and cyclin dependent kinase 2 (CDK2) in HCC. Correlations between the expression of TPT1-AS1 and CDK2 were analyzed by linear regression. TPT1-AS1 and CDK2 were overexpressed in SNU-398 and SU.86.86 cells to explore their relationship. The role of TPT1-AS1 and CDK2 in regulating the cell cycle progression and proliferation of SNU-398 and SU.86.86 cells was explored by cell cycle assay and cell proliferation assay, respectively. In addition, xenograft tumor formation was also carried out to further verify the TPT1-AS1 role in HCC in vivo. It was found that TPT1-AS1 was downregulated in HCC and inversely correlated with CDK2. The expression of TPT1-AS1 in HCC tissues was not affected by age, sex, AFP, HBV, HCV, and cirrhosis infection but was downregulated by clinical stages. In HCC cells, overexpression of TPT1-AS1 mediated the downregulation of CDK2, while silencing of TPT1-AS1 mediated the upregulation of CDK2. In cell proliferation assay, overexpression of TPT1-AS1 mediated the decreased proliferation rates, while silencing of TPT1-AS1 mediated the increased proliferation rates of HCC cells, while overexpression of CDK2 played an opposite role. In addition, overexpression of TPT1-AS1 reduced tumor growth in vivo. Therefore, overexpression of TPT1-AS1 may suppress HCC cell proliferation by downregulating CDK2.
摘要：
TPT1反义RNA1（TPT1-AS1）是最近在卵巢癌和宫颈癌中发现的肿瘤致癌长链非编码RNA（lncRNA）。本研究旨在研究lncRNATPT1-AS1在肝细胞癌（HCC）中的作用。对来自62例HCC患者的HCC和非肿瘤组织样品进行RNA分离和逆转录定量聚合酶链反应，以检测TPT1-AS1和细胞周期蛋白依赖性激酶2（CDK2）在HCC中的差异表达。通过线性回归分析TPT1-AS1和CDK2的表达之间的相关性。在SNU-398和SU.86.86细胞中过表达TPT1-AS1和CDK2以探讨它们之间的关系。通过细胞周期试验和细胞增殖试验探讨了TPT1-AS1和CDK2在调控SNU-398和SU.86.86细胞细胞周期进程和增殖中的作用,分别。此外,还进行了异种移植肿瘤形成以进一步验证TPT1-AS1在体内HCC中的作用。发现TPT1-AS1在HCC中下调，并与CDK2负相关。TPT1-AS1在肝癌组织中的表达不受年龄的影响,性别,法新社,HBV,HCV,和肝硬化感染，但被临床分期下调。在HCC细胞中，TPT1-AS1的过表达介导CDK2的下调，而TPT1-AS1的沉默介导CDK2的上调。在细胞增殖试验中,过表达TPT1-AS1介导的增殖率降低，而沉默的TPT1-AS1介导的肝癌细胞的增殖率增加，而CDK2的过表达则起相反的作用。此外,TPT1-AS1的过表达降低了体内肿瘤的生长。因此,TPT1-AS1的过表达可能通过下调CDK2抑制HCC细胞增殖。
