Long non-coding RNA LEISA promotes progression of lung adenocarcinoma via enhancing interaction between STAT3 and IL-6 promoter.


Journal

Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562

Informations de publication

Date de publication:
05 2021
Historique:
received: 08 11 2020
accepted: 23 03 2021
revised: 09 03 2021
pubmed: 17 4 2021
medline: 13 1 2022
entrez: 16 4 2021
Statut: ppublish

Résumé

Long non-coding RNAs (lncRNAs) are emerging as a new class of regulators for a variety of biological processes and have been suggested to play pivotal roles in cancer development and progression. Our current study found that a lncRNA, designated enhancing IL-6/STAT3 signaling activation (LEISA, ENST00000603468), functioned as an oncogenic lncRNA in lung adenocarcinoma (LAD), a major form of non-small cell lung carcinoma, which is one of the most frequently diagnosed malignancies with high morbidity and mortality worldwide, and was involved in the regulation of STAT3 induced IL-6 transcription. Our data showed that LEISA was highly expressed in, and correlated with the clinical progression and prognosis of LAD. Ectopic expression of LEISA promoted the proliferation and suppressed apoptosis of LAD cells in vitro and in vivo. Mechanistically, we demonstrated that LEISA recruited STAT3 to bind the promoter of IL-6 and upregulated IL-6 expression. Taken together, our work identifies LEISA as a potential diagnostic biomarker and therapeutic target for LAD.

Identifiants

pubmed: 33859372
doi: 10.1038/s41388-021-01769-7
pii: 10.1038/s41388-021-01769-7
doi:

Substances chimiques

IL6 protein, human 0
Interleukin-6 0
RNA, Long Noncoding 0
STAT3 Transcription Factor 0
STAT3 protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3449-3459

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Auteurs

Shanshan Wu (S)

Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
Department of Biology, School of Basic Medical Science, Guangdong Medical University, Zhanjiang, Guangdong, China.

Bangdong Liu (B)

Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.

Youhong Zhang (Y)

School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong, China.

Ruohui Hong (R)

Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.

Shihua Liu (S)

Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.

Tao Xiang (T)

Department of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.

Tianyu Tao (T)

Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.

Junchao Cai (J)

Department of Immunology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.

Jueheng Wu (J)

Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China. wujh@mail.sysu.edu.cn.

Mengfeng Li (M)

Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China. limf@mail.sysu.edu.cn.
School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong, China. limf@mail.sysu.edu.cn.

Hongyu Guan (H)

Department of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China. ghongy@mail.sysu.edu.cn.

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