Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, P.R. China.
Cancer Med. 2020 Nov;9(22):8600-8611. doi: 10.1002/cam4.3463. Epub 2020 Oct 2.
Esophageal cancer is one of the leading causes of cancer-related deaths worldwide. FAM225A is a novel lncRNA, only has been explored in nasopharyngeal carcinoma tumorigenesis. This study aims to investigate the regulatory mechanism of FAM225A in esophageal squamous cell carcinoma (ESCC). We discovered that FAM225A exhibited higher expression in ESCC. The silence of FAM225A attenuated cell viability, migration, and invasion, but facilitated cell apoptosis in ESCC. Exosome-mediated transfer of lncRNA FAM225A could participate in ESCC progression. In addition, we found that miR-206 bound to FAM225A. Moreover, we further demonstrated that FAM225A absorbed miR-206 to upregulate NETO2 and FOXP1 expression, and FOXP1 acted as a transcription factor to enhance FAM225A expression. Eventually, it was revealed that the overexpression of NETO2 or FOXP1 rescued the effects of FAM225A repression on ESCC progression. Our results suggested that FAM225A upregulated NETO2 and FOXP1 expression by sponging miR-206 to accelerate ESCC progression and angiogenesis. These results determined the biological role of lncRNA FAM225A in ESCC tumorigenesis, and FAM225A may be a promising biomarker for ESCC treatment.
食管癌是全球癌症相关死亡的主要原因之一。FAM225A 是一种新的 lncRNA，仅在鼻咽癌发生中得到了探索。本研究旨在探讨 FAM225A 在食管鳞状细胞癌（ESCC）中的调控机制。我们发现 FAM225A 在 ESCC 中表达较高。沉默 FAM225A 可减弱细胞活力、迁移和侵袭，但促进 ESCC 细胞凋亡。lncRNA FAM225A 的外泌体介导转移可参与 ESCC 进展。此外，我们发现 miR-206 与 FAM225A 结合。此外，我们进一步证明 FAM225A 吸收 miR-206 以上调 NETO2 和 FOXP1 的表达，FOXP1 作为转录因子增强 FAM225A 的表达。最终，结果表明，NETO2 或 FOXP1 的过表达可挽救 FAM225A 抑制对 ESCC 进展的影响。我们的结果表明，FAM225A 通过海绵 miR-206 上调 NETO2 和 FOXP1 的表达，从而加速 ESCC 的进展和血管生成。这些结果确定了 lncRNA FAM225A 在 ESCC 肿瘤发生中的生物学作用，并且 FAM225A 可能是 ESCC 治疗的有前途的生物标志物。
