Effect of small nuclear ribonucleoprotein polypeptide A on the malignant biological behavior of hepatocellular carcinoma cells and its mechanism / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探究小核核糖核蛋白多肽A（SNRPA）在肝细胞癌（HCC）组织和细胞中的表达及其调控HCC细胞HepG2和Hep3B恶性生物学行为的作用及其机制。方法: 数据库分析SNRPA在泛癌组织中的表达及其与病理分期、HCC患者预后的相关性。常规培养HepG2和Hep3B细胞，将si-NC，si-SNRPA#1、si-SNRPA#2转染HepG2和Hep3B细胞，实验分为si-NC组、si-SNRPA#1组和si-SNRPA#2组；将SNRPA-vector和SNRPA-oe载体转染LO2细胞，分为SNRPA-vector组和SNRPA-oe组。qPCR法检测正常肝细胞和肝癌细胞以及转染各组HepG2和Hep3B细胞中SNRPA mRNA的表达，MTT法、Transwell法和WB法分别检测转染后各组HepG2和Hep3B细胞的增殖、迁移和侵袭能力以及EMT相关蛋白表达的变化。结果: 数据库分析显示，SNRPA mRNA在多数肿瘤组织中均呈高表达（均P<0.001）且与病理分期有关联（P<0.05或P<0.01）。SNRPA在HCC组织和细胞中均呈高表达（P<0.05或P<0.01），且与HCC患者的预后有关联（P<0.01）。敲减SNRPA表达明显抑制HepG2和Hep3B细胞增殖（P<0.05或P<0.01）而过表达SNRPA则能促进LO2细胞增殖（P<0.01），敲减SNRPA表达明显抑制HepG2和Hep3B细胞的迁移和侵袭能力（均P<0.01），明显促进E-cadherin的表达上调（P<0.01），而抑制N-cadherin、vimentin的表达（P<0.01）。结论: SNRPA在HCC组织及细胞中呈明显高表达，其可能通过调控上皮间质转化（EMT）进程进而促进HepG2和Hep3B细胞的增殖、迁移和侵袭。

Role of lncRNA SNHG5 in the migration and invasion of hypoxia-induced hyhepa‐ tocellular carcinoma cells / 中国肿瘤生物治疗杂志

@#[Abstract] Objective: To explore the regulatory effect of long non-coding RNA (lncRNA) SNHG5 on invasion and migration of hypoxia-induced hepatocellular carcinoma (HCC) cells. Methods: A total of 20 pairs of cancer and para-cancerous tissue specimens resected from HCC patients in the First Affiliated Hospital of Xi'an Jiaotong University from January 2017 to June 2018, and human HCC cell lines (HepG2, MHCC-97L, MHCC-97H , Huh7) as well as immortalized human liver LO2 cells were collected for this study. Bioinformatics methods were used to analyze the binding sites between hypoxia-inducible factor 1α (HIF-1α) and SNHG5. pCMVHIF-1α and shRNA-SNHG5 (sh-SNHG5) plasmids were transfected into HCC cells, respectively. qPCR was used to detect the expres‐ sion level of SNHG5 in HCC tissues and hypoxia-induced HCC cells. Western botting was used to detect the expression level of HIF-1α protein in HCC cells, and Transwell chamber method was used to detect the migration and invasion ability of HCC cells after SNHG5 si‐ lence under normoxia and hypoxia condition. Results: Compared with para-cancerous tissues and immortalized human liver LO2 cells, the expression of SNHG5 was significantly up-regulated in HCC tissues and cell lines (all P<0.01). Hypoxia promoted the expression level of SNHG5 in HCC cells, and its mechanism might be related to the combination of hypoxia-activated HIF-1α and SNHG5 promoter to promote its transcription. Hypoxia promoted the invasion and migration ability of HepG2 and MHCC-97L cells (all P< 0.01), but knockdown of SNHG5 significantly inhibited the invasion and migration ability of HepG2 and MHCC-97L cells under hy‐ poxic conditions (all P<0.01). Conclusion: SNHG5 is highly expressed in HCC tissues and cell lines and plays an important role in the invasion and migration of HCC cells induced by hypoxia.