Evidence shows that long noncoding RNAs (lncRNAs) modulate mRNAs of multiple genes by post-transcriptional regulation. However, in esophageal squamous cell carcinoma, lncRNAs involvement in post-transcriptional regulation of mRNAs have been rarely reported. In this study, we investigated a novel mechanism of linc01305 promoting metastasis and proliferation of ESCC. The results for real-time quantitative reverse transcription PCR (qRT-PCR) and fluorescence in situ hybridization showed that linc01305 was highly expressed and predominantly located in cytoplasm of human esophageal cancer cells. Transwell and colony formation assays confirmed that linc01305 promoted migration and proliferation of esophageal cancer cells. RNA-seq, linc01305 pulldown, mass spectrometry, RNA immunoprecipitation and mRNA stability assays demonstrated that linc01305 stabilized mRNA of target gene HTR3A through interacting with IGF2BP2 and IGF2BP3. Taken together, our data unveils a novel mechanism in which cytoplasmic linc01305 stabilizes HTR3A mRNA through interacting with IGF2BP2 and IGF2BP3 and thereby promotes metastasis and proliferation of ESCC.

有证据表明，长链非编码 RNA (lncRNA) 通过转录后调控来调节多个基因的 mRNA。然而，在食管鳞状细胞癌中，很少报道lncRNAs参与mRNAs的转录后调控。在这项研究中，我们研究了 linc01305 促进 ESCC 转移和增殖的新机制。实时定量逆转录 PCR (qRT-PCR) 和原位荧光的结果杂交显示linc01305高表达，主要位于人食管癌细胞的细胞质中。Transwell 和集落形成试验证实 linc01305 促进食管癌细胞的迁移和增殖。RNA-seq、linc01305 pulldown、质谱、RNA免疫沉淀和mRNA稳定性测定表明linc01305通过与IGF2BP2和IGF2BP3相互作用稳定靶基因HTR3A的mRNA。总之，我们的数据揭示了一种新机制，其中细胞质 linc01305 通过与 IGF2BP2 和 IGF2BP3 相互作用稳定 HTR3A mRNA，从而促进 ESCC 的转移和增殖。