Esophageal cancer (EC) is a malignancy causing lots of mortality worldwide. Long non-coding RNAs (lncRNAs) are involved in the progression of multiple cancer types. The present study aimed to explore the function and associated mechanisms of lncRNA metastasis-associated lung adenocarcinoma transcript1 (MALAT1) in EC development by focusing on its interaction with miR-1-3p. The levels of MALAT1 and miR-1-3p were investigated in clinical EC specimens. Then, the expression of MALAT1 was knocked down in EC cell lines, and the effects of MALAT1 inhibition on the viability, migration, and invasion, and miR-1-3p/Coronin-1C (CORO1C)/Tropomyosin3 (TPM3) axis in EC cells were detected. The interaction between MALAT1 and miR-1-3p in the progression of EC was further determined by suppressing the expression of miR-1-3p in MALAT1 inhibition cells. The results were further verified with EC xenograft mice model. MALAT1 level was downregulated, while miR-1-3p level was upregulated in EC specimens. The inhibition of MALAT1 suppressed the viability, migration, and invasion in EC cell lines. The changes in phenotypes of EC cells were associated with the upregulation of miR-1-3p level and inhibition of CORO1C/TPM3 activity. Furthermore, the results of dual-luciferase assay showed the direct binding of MALAT1 to the seed sequence of miR-1-3p. The suppressed level of miR-1-3p not only induced the activity of CORO1C/TPM3 signaling, but also upregulated MALAT1 expression, indicating the reciprocal regulation between the two factors. The inhibition of MALAT1 also inhibited tumor growth and epithelial-mesenchymal transition (EMT) in mice model, which was reversed by miR-1-3p inhibition. Collectively, MALAT1 was important to the survival and metastasis of EC cells by sponging miR-1-3p.

食道癌（EC）是一种恶性肿瘤，在全球范围内导致大量死亡。长的非编码RNA（lncRNA）参与多种癌症类型的进展。本研究旨在探讨lncRNA转移相关的肺腺癌转录物1（MALAT1）在EC发育中的功能及相关机制，重点是与miR-1-3p的相互作用。在临床EC标本中研究了MALAT1和miR-1-3p的水平。然后，敲低MALAT1在EC细胞系中的表达，并抑制MALAT1对存活，迁移和侵袭以及miR-1-3p / Coronin-1C（CORO1C）/ Tropomyosin3（TPM3）轴的影响检测到细胞。通过抑制MALAT1抑制细胞中miR-1-3p的表达，进一步确定MALAT1和miR-1-3p在EC进程中的相互作用。EC异种移植小鼠模型进一步验证了结果。EC标本中MALAT1水平下调，而miR-1-3p水平上调。MALAT1的抑制作用抑制了EC细胞系的活力，迁移和侵袭。EC细胞表型的变化与miR-1-3p水平的上调和CORO1C / TPM3活性的抑制有关。此外，双荧光素酶测定的结果表明MALAT1与miR-1-3p的种子序列直接结合。抑制水平的miR-1-3p不仅诱导CORO1C / TPM3信号传导活性，而且上调MALAT1表达，表明这两个因素之间存在相互调节作用。MALAT1的抑制作用还抑制了小鼠模型中的肿瘤生长和上皮-间质转化（EMT），而miR-1-3p抑制作用则逆转了这种情况。总的来说，