目的：探讨富含丝氨酸/精氨酸剪接因子7（SRSF7）对肝细胞癌（HCC）细胞HepG2增殖、迁移和侵袭的影响及其可能 机制。方法：通过癌症基因组图谱（TCGA）和Kaplan-Meier Plotter在线分析SRSF7在HCC和癌旁组织中的差异表达及其与患 者预后的关系。常规培养HepG2细胞，用转染试剂将SRSF7 RNA敲减序列（siSRSF7#1和siSRSF7#2）、对照序列（NC）、SRSF7过 表达载体（hSRSF7-oe）和对照载体（hSRSF7-nc）转染至 HepG2 细胞中，实验分为 NC 组、siSRSF7#1 组、siSRSF7#2 组、NC + hSRSF7-nc组、siSRSF7 + hSRSF7-nc组和siSRSF7 + hSRSF7-oe组。通过qPCR和WB法检测各组HepG2细胞中SRSF7 mRNA 和蛋白的表达，MTS实验、平板克隆形成实验、划痕愈合实验、Transwell小室实验分别检测各组HepG2细胞的增殖、迁移和侵袭 的能力。WB法检测各组HepG2细胞中JAK1/STAT3信号通路的相关蛋白的表达。结果：数据库数据分析显示SRSF7 mRNA在 HCC组织中呈高表达（P < 0.001），SRSF7 mRNA高表达与HCC患者不良预后有关联（P < 0.05）。敲减SRSF7后，HepG2细胞的 增殖、迁移和侵袭能力均显著下降（均P < 0.01）。敲减SRSF7组细胞中JAK1和STAT3磷酸化水平显著降低（均P < 0.05），同时过 表达SRSF7后，JAK1和STAT3磷酸化水平又明显升高（均P < 0.05）。结论：SRSF7在HCC组织中呈高表达，其可能通过调控 JAK1/STAT3信号通路促进HepG2细胞的增殖、迁移和侵袭。

Objective: To investigate the effects of serine/arginine-rich splicing factor 7 (SRSF7) on proliferation, migration and invasion of hepatocellular carcinoma (HCC) HepG2 cells and the possible mechanisms. Methods: Differential expression of SRSF7 between HCC and adjacent non-tumor tissues and its relationship with patient prognosis were analyzed online using The Cancer Genome Atlas (TCGA) and Kaplan Meier Plotter. HepG2 cells were cultured routinely and transfected with SRSF7 RNA knockdown sequences (siSRSF7#1 and siSRSF7#2), control sequences (NC), SRSF7 overexpression vector (hSRSF7-oe), and control vector (hSRSF7-nc) using transfection reagents. Accordingly, the cells were divided into NC group, siSRSF7#1 group, siSRSF7#2 group, NC + hSRSF7-nc group, siSRSF7 + hSRSF7-nc group, and siSRSF7 + hSRSF7-oe group. The mRNA and protein expression levels of SRSF7 in each group of cells were detected by qPCR and WB assay. The proliferation, migration, and invasion abilities of each group of cells were assessed by MTS assay, plate clone formation assay, scratch assay, and Transwell invasion assay. WB assay was used to detect the expression of JAK1/STAT3 signaling pathway related proteins in HepG2 cells of each group. Results: Database analysis showed that SRSF7 mRNA is highly expressed in HCC tissues (P < 0.001), and its high expression is associated with poor prognosis in HCC patients (P < 0.05). Knockdown of SRSF7 significantly reduced the proliferation, migration, and invasion abilities of HepG2 cells (all P < 0.01). The phosphorylation levels of JAK1 and STAT3 in the SRSF7 knockdown cells were significantly reduced (both P < 0.05), while overexpression of SRSF7 resulted in a significant increase in JAK1 and STAT3 phosphorylation levels (both P < 0.05). Conclusion: SRSF7 is highly expressed in HCC tissues and may promote the proliferation, migration, and invasion of HepG2 cells by regulating the JAK1/STAT3 signaling pathway.

河北省高等学校科学研究计划（No. ZD2022011）；河北省自然科学基金（No. H2020208002，No. H2019208216）