LINC01305 recruits basonuclin 1 to act on G‐protein pathway suppressor 1 to promote esophageal squamous cell carcinoma

• Published in: Cancer science Vol. 114; no. 11; pp. 4314 - 4328
• Main Authors: Xiong, Li, Tan, Jinsong, Zhang, Ruolan, Long, Qiongxian, Xiong, Rong, Liu, Yanqun, Liu, Yun, Tang, Jiancai, Li, Yan, Feng, Gang, Song, Guiqin, Liu, Kang
• Format: Journal Article
• Language: English
• Published: Tokyo John Wiley & Sons, Inc 01.11.2023; John Wiley and Sons Inc
• Subjects: Basonuclin; Biotechnology; Cells; Esophageal cancer; Esophageal carcinoma; Genes; Medical prognosis; Metastases; Metastasis; Molecular modelling; Original; Plasmids; Proteins; Signal transduction; Squamous cell carcinoma; Therapeutic targets; Transcription factors
• ISSN: 1347-9032; 1349-7006
• DOI: 10.1111/cas.15963

EsophageaL squamous cell carcinoma (ESCC) is one of the most common and lethal tumors, however, its underlying molecular mechanisms are not completely understood and new therapeutic targets are needed. Here, we found that the transcription factor basonuclin 1 (BNC1) was significantly upregulated and closely related to the differentiation and metastasis of ESCC. Furthermore, BNC1, LINC01305, and G-protein pathway suppressor 1 (GPS1) had significant oncogenic roles in ESCC. In addition, in vivo experiments showed that knockdown of BNC1 indeed significantly inhibited the proliferation and metastasis of ESCC. We also revealed the molecular mechanism by which LINC01305 recruits BNC1 to the promoter of GPS1, and then GPS1 could mediate the JNK signaling pathway to promote the proliferation and metastases of ESCC. Taken together, we discovered the novel molecular mechanism by which LINC01305/BNC1 upregulates GPS1 expression to promote the development of ESCC, providing a new therapeutic target for ESCC.