Long non‐coding RNAs (lncRNAs) have been well demonstrated to emerge as crucial regulators in cancer progression, and they can function as regulatory network based on their interactions. Although the biological functions of FAM83H‐AS1 have been confirmed in various tumour progressions, the underlying molecular mechanisms of FAM83H‐AS1 in oesophageal squamous cell carcinoma (ESCC) remained poorly understood. To address this, we treated human oesophageal cancer cell line Eca109 cells with TGF‐β and found FAM83H‐AS1 was notably overexpressed. In the present study, FAM83H‐AS1 was observed to be significantly up‐regulated in ESCC tissues and was associated with TNM stage, pathological differentiation and lymph node metastasis. FAM83H‐AS1 reinforced oesophageal cancer cell proliferation, migration and invasion, and participated in epithelial‐to‐mesenchymal transition (EMT) process at mRNA and protein levels. In addition, a concordant regulation between FAM83H‐AS1 and its sense strand FAM83H was detected at the transcriptional and translational levels. Furthermore, FAM83H‐AS1 could act as competing endogenous RNA to affect the expression of Girdin by sponging miR‐10a‐5p verified by RIP and luciferase reporter assays. Consequently, the study provided a unique perspective of FAM83H‐AS1 in ESCC progression, which may be considered as potential biomarker and therapeutic target for ESCC therapy.

中文翻译：

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LncRNA FAM83H-AS1通过miR-10a-5p / Girdin轴促进食道鳞状细胞癌的进展。

长非编码RNA（lncRNA）已被证明是癌症进展中的关键调节因子，它们可以基于它们的相互作用起调节网络的作用。尽管已在各种肿瘤进展中证实了FAM83H-AS1的生物学功能，但对食管鳞状细胞癌（ESCC）中FAM83H-AS1的潜在分子机制仍知之甚少。为了解决这个问题，我们用TGF-β处理了人食道癌细胞系Eca109，发现FAM83H-AS1明显过表达。在本研究中，观察到FAM83H-AS1在ESCC组织中显着上调，并与TNM分期，病理分化和淋巴结转移有关。FAM83H‐AS1增强了食道癌细胞的增殖，迁移和侵袭，并参与了mRNA和蛋白质水平的上皮-间质转化（EMT）过程。另外，在转录和翻译水平上检测到FAM83H-AS1及其有义链FAM83H之间的一致调控。此外，FAM83H-AS1可以通过竞争经RIP和荧光素酶报告基因检测证实的miR-10a-5p作为竞争性内源RNA来影响Girdin的表达。因此，该研究为FAM83H-AS1在ESCC进展中提供了独特的视角，可将其视为ESCC治疗的潜在生物标志物和治疗靶标。FAM83H‐AS1可以通过竞争经RIP和荧光素酶报告基因检测证实的miR‐10a‐5p作为竞争性内源RNA来影响Girdin的表达。因此，该研究为FAM83H-AS1在ESCC进展中提供了独特的视角，可将其视为ESCC治疗的潜在生物标志物和治疗靶标。FAM83H‐AS1可以通过竞争经RIP和荧光素酶报告基因检测证实的miR‐10a‐5p作为竞争性内源RNA来影响Girdin的表达。因此，该研究为FAM83H-AS1在ESCC进展中提供了独特的视角，可将其视为ESCC治疗的潜在生物标志物和治疗靶标。