目的：探讨长片段非编码RNA（lncRNA）MALAT1 在肝癌中的表达及其的功能。方法：用qRT-PCR 方法检测80 例肝癌患者手术切除的癌组织及其癌旁组织，以及不同肝癌细胞系（HepG2、Hep3B、HCCLM3、HuH7）与正常肝细胞系（L02）中MALAT1 的表达。分别用MTT 试验、划痕试验、流式细胞术检测肝癌细胞（HepG2、HuH7）转染MALAT1 siRNA 后增殖、迁移、凋亡的变化。结果：80 例配对标本中，72 例（90%）肝癌组织MALAT1 表达较其癌旁组织明显上调，MALAT1在不同肝癌细胞系中的表达水平均不同程度明显高于正常肝癌细胞（均P<0.05）；HepG2、HuH7转染MALAT1 siRNA 后，增殖率均呈时间依赖性降低、划痕愈合能力均明显减弱（均P<0.05），细胞凋亡率分别为17.0%、16.41%，而各自的对照组分别为8.89%、6.56%，差异有统计学意义（P<0.05）。结论：MALAT1 在肝癌中的表达上调，且可能与肝癌的恶性生物学行为密切相关，对其作用机制的进一步研究，有望为肝癌的治疗找到新的靶点。
Long non-coding RNA MALAT1 expression in hepatocellular carcinoma and its action
Objective: To investigate the long non-coding RNA (lncRNA) MALAT1 expression in hepatocellular carcinoma (HCC) and its function. Methods: The MALAT1 expressions in 80 surgical specimens consisting of tumor and adjacent normal tissue as well as in different HCC cells lines (HepG2, Hep3B, HCCLM3, and HuH7) and normal hepatic cell line (L02) were determined by qRT-PCR method. The changes in proliferation, migration and apoptosis in HCC cells (HepG2 and HuH7) after MALAT1 siRNA transfection were examined by MTT assay, wound healing assay and flow cytometry, respectively. Results: In 72 of the 80 paired samples (90%), the MALAT1 expression in HCC tissue was significantly upregulated compared with its adjacent normal tissue, and the MALAT1 expression level in each examined HCC cell line was significantly higher to varying degrees than that in normal hepatic cell line (all P<0.05). In HepG2 and HuH7 cells after MALAT1 siRNA transfection, the proliferation rate was significantly decreased in a timedependent manner, wound healing ability was significantly weakened (all P<0.05), the apoptosis rate was 17.0% and 16.41%, which in their corresponding group was 8.89% and 6.56% respectively, and the difference had statistical significance (both P<0.05). Conclusion: MALAT1 expression is up-regulated in HCC, which may be closely associated with the malignant behaviors of HCC, and further investigation of its action mechanism may probably uncover a potential new therapeutic target for HCC.