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THAP9-AS1/miR-133b/SOX4 正反馈环路促进食管鳞癌细胞的进展。

THAP9-AS1/miR-133b/SOX4 positive feedback loop facilitates the progression of esophageal squamous cell carcinoma.

机构信息

Department of Thoracic Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, 450008, Zhengzhou, China.

出版信息

Cell Death Dis. 2021 Apr 14;12(4):401. doi: 10.1038/s41419-021-03690-z.

DOI:10.1038/s41419-021-03690-z
PMID:33854048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8046801/
Abstract

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors in the digestive system with a high incidence and poor prognosis. Long non-coding RNAs (LncRNA) have been reported to be closely associated with the occurrence and development of various human cancers. Data from GSE89102 shows an increase of THAP9-AS1 expression in ESCC. However, its functions and mechanisms underlying ESCC progression remain to be investigated. In this study, we found that THAP9-AS1 was overexpressed in ESCC tissues and cells. High THAP9-AS1 expression was positively correlated with tumor size, TNM stage, lymph node metastasis, and worse prognosis. Functionally, depletion of THAP9-AS1 suppressed cell proliferation, migration, and invasion, while enhanced apoptosis in vitro. Consistently, knockdown of THAP9-AS1 inhibited xenograft tumor growth in vivo. Mechanistically, THAP9-AS1 could serve as a competing endogenous RNA (ceRNA) for miR-133b, resulting in the upregulation of SOX4. Reciprocally, SOX4 bound to the promoter region of THAP9-AS1 to activate its transcription. Moreover, the anti-tumor property induced by THAP9-AS1 knockdown was significantly impaired due to miR-133b downregulation or SOX4 overexpression. Taken together, our study reveals a positive feedback loop of THAP9-AS1/miR-133b/SOX4 to facilitate ESCC progression, providing a potential molecular target to fight against ESCC.

摘要

食管鳞状细胞癌 (ESCC) 是消化系统中最常见的恶性肿瘤之一，发病率高，预后差。长链非编码 RNA (LncRNA) 已被报道与多种人类癌症的发生和发展密切相关。来自 GSE89102 的数据显示，THAP9-AS1 在 ESCC 中的表达增加。然而，其在 ESCC 进展中的功能和机制仍有待研究。在本研究中，我们发现 THAP9-AS1 在 ESCC 组织和细胞中表达上调。高 THAP9-AS1 表达与肿瘤大小、TNM 分期、淋巴结转移和预后不良呈正相关。功能上，THAP9-AS1 的耗竭抑制了细胞增殖、迁移和侵袭，同时增强了体外细胞凋亡。一致地，THAP9-AS1 的敲低抑制了体内异种移植肿瘤的生长。机制上，THAP9-AS1 可以作为 miR-133b 的竞争性内源 RNA (ceRNA)，导致 SOX4 的上调。反过来，SOX4 结合到 THAP9-AS1 的启动子区域以激活其转录。此外，由于 miR-133b 的下调或 SOX4 的过表达，THAP9-AS1 敲低诱导的抗肿瘤特性明显受损。总之，我们的研究揭示了 THAP9-AS1/miR-133b/SOX4 的正反馈环促进 ESCC 进展，为对抗 ESCC 提供了一个潜在的分子靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/553d53a8e747/41419_2021_3690_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/4bc16d928645/41419_2021_3690_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/5ba0c4250f52/41419_2021_3690_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/1d34d928b657/41419_2021_3690_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/8d9e45b45c8c/41419_2021_3690_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/5b0d5db170e7/41419_2021_3690_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/32ef128b5916/41419_2021_3690_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/0590ff291cbe/41419_2021_3690_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/553d53a8e747/41419_2021_3690_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/4bc16d928645/41419_2021_3690_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/5ba0c4250f52/41419_2021_3690_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/1d34d928b657/41419_2021_3690_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/8d9e45b45c8c/41419_2021_3690_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/5b0d5db170e7/41419_2021_3690_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/32ef128b5916/41419_2021_3690_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/0590ff291cbe/41419_2021_3690_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b073/8046801/553d53a8e747/41419_2021_3690_Fig8_HTML.jpg

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