Wang Juan, Zhou Yuan, Gu Chunyan, Ming Fang, Zhang Ying
Department of Infectious Disease, Nantong Third Affiliated Hospital of Nantong University, Nantong, China.
Department of Hepatobiliary Surgery, Tumor Hospital Affiliated to Nantong University, Nantong Tumor Hospital, Nantong, China.
J Oncol. 2022 Aug 23;2022:9096365. doi: 10.1155/2022/9096365. eCollection 2022.
Assessment of lncRNA SAMD12-AS1 expression in liver cancer tissues and cell lines to investigate the underlying molecular mechanisms that regulate liver cancer cell growth, development, invasion, and migration.
The lncRNA SAMD12-AS1 expression in tumor tissues of 32 liver cancer patients was measured by real-time PCR, and its effect on the clinicopathological manifestations and liver cancer patients' prognosis was determined. LncRNA SAMD12-AS1 overexpression and knockdown in liver cancer cell lines were established by cell transfection. The effects of lncRNA SAMD12-AS1 knockdown and overexpression on liver cancer cell growth, development, invasion, and migration were determined by MTT, Transwell, and clonogenic assays. Furthermore, its effects on the expression of E-cadherin, vimentin, p53, and p21 in hepatocellular carcinoma cells were determined by Western blot assay.
The level of lncRNA SAMD12-AS1 expression in tumor tissues was remarkably higher than that in paracancerous liver tissues ( < 0.01). It was found that the lncRNA SAMD12-AS1 expression was largely correlated with TNM stage of tumor, vascular invasion, and hepatitis B surface (HBs) antigen in liver cancer patients ( < 0.05). Cell function experiments showed that lncRNA SAMD12-AS1 overexpression promoted liver cancer development, migration, and invasion ( < 0.05), while lncRNA SAMD12-AS1 knockdown inhibited the activity of liver cancer cells to invade and migrate ( < 0.05). Western blot analysis showed that overexpression of lncRNA SAMD12-AS1 markedly inhibited p21, p53, and E-cadherin expression and promoted vimentin expression. Conversely, knockdown of lncRNA SAMD12-AS1 significantly promoted p21, p53, and E-cadherin expression and inhibited vimentin expression ( < 0.05).
LncRNA SAMD12-AS1 is associated with the TNM stage and vascular invasion of liver cancer. It promotes liver cancer cell development, invasion, and migration by regulating p53 expression. Thus, lncRNA SAMD12-AS1 could be a novel biological target for the treatment of liver cancer.
评估lncRNA SAMD12-AS1在肝癌组织和细胞系中的表达，以探究调节肝癌细胞生长、发育、侵袭和迁移的潜在分子机制。
采用实时荧光定量PCR检测32例肝癌患者肿瘤组织中lncRNA SAMD12-AS1的表达，并确定其对临床病理表现和肝癌患者预后的影响。通过细胞转染建立lncRNA SAMD12-AS1在肝癌细胞系中的过表达和敲低模型。采用MTT法、Transwell法和克隆形成实验确定lncRNA SAMD12-AS1敲低和过表达对肝癌细胞生长、发育、侵袭和迁移的影响。此外，通过蛋白质免疫印迹法检测其对肝癌细胞中E-钙黏蛋白、波形蛋白、p53和p21表达的影响。
肿瘤组织中lncRNA SAMD12-AS1的表达水平显著高于癌旁肝组织（<0.01）。发现lncRNA SAMD12-AS1的表达与肝癌患者的肿瘤TNM分期、血管侵犯和乙肝表面（HBs）抗原密切相关（<0.05）。细胞功能实验表明，lncRNA SAMD12-AS1过表达促进肝癌的发展、迁移和侵袭（<0.05），而lncRNA SAMD12-AS1敲低则抑制肝癌细胞的侵袭和迁移活性（<0.05）。蛋白质免疫印迹分析表明，lncRNA SAMD12-AS1过表达显著抑制p21、p53和E-钙黏蛋白的表达，促进波形蛋白的表达。相反，lncRNA SAMD12-AS1敲低显著促进p21、p53和E-钙黏蛋白的表达，抑制波形蛋白的表达（<0.05）。
lncRNA SAMD12-AS1与肝癌的TNM分期和血管侵犯有关。它通过调节p53表达促进肝癌细胞的发展、侵袭和迁移。因此，lncRNA SAMD12-AS1可能是治疗肝癌的新型生物学靶点。
