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Archive > Volume 31 Issue 9 > 2024,31(9):864-870. DOI:10.3872/j.issn.1007-385X.2024.09.004 Prev Next
Basic Research
The effects and possible mechanisms of SRSF7 on the proliferation, migration, and invasion of HepG2 cells
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Abstract:
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.
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