LncRNA LUESCC promotes esophageal squamous cell carcinoma by targeting the miR-6785-5p/NRSN2 axis

Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent gastrointestinal malignancies with high mortality worldwide. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in human cancers, including ESCC. However, the detailed mechanisms of lncRNAs in the regulat...

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Published inCellular and molecular life sciences : CMLS Vol. 81; no. 1; p. 121
Main Authors Xue, Song-tao, Cao, Shi-qiang, Ding, Jian-cheng, Li, Wen-juan, Hu, Guo-sheng, Zheng, Jian-cong, Lin, Xiao, Chen, Chun, Liu, Wen, Zheng, Bin
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.12.2024
Springer Nature B.V
Subjects
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cancer
Cell Biology
Cell migration
Cell proliferation
Cytoplasm
Esophageal cancer
Esophageal carcinoma
gastrointestinal system
gender
humans
In vivo methods and tests
Life Sciences
Lymph nodes
Malignancy
Metastases
metastasis
mortality
Non-coding RNA
Original
Original Article
prognosis
Squamous cell carcinoma
Therapeutic targets
therapeutics
LUESCC
NRSN2
miR-6785-5p
CeRNA
ASO
ESCC
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Summary:Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent gastrointestinal malignancies with high mortality worldwide. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in human cancers, including ESCC. However, the detailed mechanisms of lncRNAs in the regulation of ESCC progression remain incompletely understood. LUESCC was upregulated in ESCC tissues compared with adjacent normal tissues, which was associated with gender, deep invasion, lymph node metastasis, and poor prognosis of ESCC patients. LUESCC was mainly localized in the cytoplasm of ESCC cells. Knockdown of LUESCC inhibited cell proliferation, colony formation, migration, and invasion in vitro and suppressed tumor growth in vivo. Mechanistic investigation indicated that LUESCC functions as a ceRNA by sponging miR-6785-5p to enhance NRSN2 expression, which is critical for the malignant behaviors of ESCC. Furthermore, ASO targeting LUESCC substantially suppressed ESCC both in vitro and in vivo. Collectively, these data demonstrate that LUESCC may exerts its oncogenic role by sponging miR-6785-5p to promote NRSN2 expression in ESCC, providing a potential diagnostic marker and therapeutic target for ESCC patients.
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ISSN:1420-682X
1420-9071
1420-9071
DOI:10.1007/s00018-024-05172-9