The expression of lncRNA ESCCAL-1 is upregulated in esophageal squamous cell carcinoma (ESCC). However, the molecular pathways regulated by ESCCAL-1 in esophageal cancer remain obscure. We found that high expression of the lncRNA ESCCAL-1 in human ESCC tumors correlated with worse clinicopathologic features. Furthermore, depletion of ESCCAL-1 in ESCC models inhibited the cellular processes associated with malignancy, including proliferation, migration and invasion, resistance to apoptosis, and impaired tumor growth in mice. Using a combinatorial approach, we discovered that ESCCAL-1 regulates malignant phenotypes in ESCC by acting as a molecular sponge for miR-590-3p. This interaction prevents miR-590-3p from suppressing APOBEC3G expression. Increased APOBEC3G was also a biomarker of worse clinicopathologic features in human ESCC tumors. Depletion of ESSCAL-1 or APOBEC3G, or overexpression of miR-590-3p resulted in increased apoptosis due to downregulation of the PI3K/Akt signaling. This study demonstrates that the lncRNA ESCCAL-1 promotes malignant features of ESCC by relieving the inhibitory effect of miR-590-3p on APOBEC3G expression and identifies potential biomarkers or therapeutic targets to improve ESCC treatment outcomes.

在食管鳞状细胞癌（ESCC）中，lncRNA ESCCAL-1的表达上调。但是，食管癌中由ESCCAL-1调控的分子途径仍然不清楚。我们发现在人类ESCC肿瘤中lncRNA ESCCAL-1的高表达与更差的临床病理特征相关。此外，ESCCC-1模型中ESCCAL-1的耗竭抑制了与恶性肿瘤相关的细胞过程，包括增殖，迁移和侵袭，对细胞凋亡的抗性以及小鼠肿瘤生长的损害。使用组合方法，我们发现ESCCAL-1通过充当miR-590-3p的分子海绵来调节ESCC中的恶性表型。这种相互作用可防止miR-590-3p抑制APOBEC3G表达。APOBEC3G升高也是人ESCC肿瘤中较差的临床病理特征的生物标志。ESSCAL-1或APOBEC3G的耗竭，或miR-590-3p的过表达，由于PI3K / Akt信号转导下调而导致凋亡增加。这项研究表明，lncRNA ESCCAL-1通过减轻miR-590-3p对APOBEC3G表达的抑制作用来促进ESCC的恶性特征，并确定潜在的生物标志物或治疗靶标，以改善ESCC的治疗结果。