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

Author:

Xiong Li12,Tan Jinsong13,Zhang Ruolan12,Long Qiongxian1,Xiong Rong12,Liu Yanqun1,Liu Yun3,Tang Jiancai3,Li Yan4,Feng Gang1,Song Guiqin3ORCID,Liu Kang12ORCID

Affiliation:

1. Institute of Tissue Engineering and Stem Cells, Nanchong Central Hospital, The Second Clinical Medical College North Sichuan Medical College Nanchong China

2. Department of Laboratory Medicine North Sichuan Medical College Nanchong China

3. Institute of Basic Medicine and Forensic Medicine North Sichuan Medical College Nanchong China

4. Department of Anatomy and Physiology, College of Basic Medical Science, Songjiang Research Institute and Songjiang Hospital Shanghai Jiao Tong University School of Medicine Shanghai China

Abstract

AbstractEsophageaL 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.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Sichuan Province

Publisher

Wiley

Subject

Cancer Research,Oncology,General Medicine

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