PMID- 34630709
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231129
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Print)
IS  - 1792-1074 (Linking)
VI  - 22
IP  - 5
DP  - 2021 Nov
TI  - Long non-coding RNA NEAT1 promotes the malignancy of laryngeal squamous cell 
      carcinoma by regulating the microRNA-204-5p/SEMA4B axis.
PG  - 802
LID - 10.3892/ol.2021.13063 [doi]
LID - 802
AB  - Laryngeal squamous cell carcinoma (LSCC) is a highly invasive malignant tumor in 
      the head and neck area. As an oncogene, long non-coding RNA (lncRNA) nuclear 
      enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and 
      invasion several types of cancer. The present study aimed to reveal the effects 
      of NEAT1 on the progression of LSCC. Reverse transcription-quantitative PCR 
      (RT-qPCR) was used to detect relative mRNA expression levels of NEAT1, microRNA 
      (miR)-204-5p and semaphorin (SEMA) 4B. Kaplan-Meier analysis was used to analyze 
      overall survival times. RNA in-situ hybridization (ISH) exhibited the 
      distribution of NEAT1 and miR-204-5p in tissues. RNA fluorescence ISH was used to 
      analyze the distribution of NEAT1 and miR-204-5p in the cells. Western blot 
      analysis was used to detect the expression level of target proteins. Cell 
      viability was analyzed using a MTT assay, while flow cytometry was used to 
      determine cell apoptosis. Wound healing and Transwell invasion assays were used 
      to value cell migration and invasion, respectively. RNA immunoprecipitation 
      assay, bioinformatics prediction and a dual luciferase reporter assay were used 
      to analyze the target relationship. The RT-qPCR results showed that NEAT1 was 
      highly expressed and miR-204-5p had decreased expression in LSCC tissues and 
      cells compared with that in the normal tissue and the 16HBE-14o cell line, 
      respectively. Knockdown of NEAT1 using small interfering (si) RNA and 
      overexpressed miR-204-5p both effectively inhibited the proliferation, migration 
      and invasion of LSCC cells. Besides, further experiments revealed that miR-204-5p 
      was a target of NEAT1. At the same time, silenced miR-204-5p reversed the 
      anti-tumor effects of si-NEAT1. In addition, SEMA4B was targeted by miR-204-5p in 
      LSCC cells and upregulated SEMA4B weakened the antitumor effects of miR-204-5p in 
      LSCC cells. NEAT1 regulated the expression of SEMA4B by targeting miR-204-5p in 
      LSCC cells. Overall, NEAT1 promoted the proliferation and invasion of LSCC cells 
      by regulating the miR-204-5p/SEMA4B axis.
CI  - Copyright: (c) Han et al.
FAU - Han, Ling
AU  - Han L
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital, The Second 
      Clinical Medical College of Jinan University, The First Affiliated Hospital of 
      Southern University of Science and Technology, Shenzhen, Guangdong 518020, P.R. 
      China.
FAU - Zheng, Chaopan
AU  - Zheng C
AD  - Department of Otorhinolaryngology, Shenzhen People's Hospital, The Second 
      Clinical Medical College of Jinan University, The First Affiliated Hospital of 
      Southern University of Science and Technology, Shenzhen, Guangdong 518020, P.R. 
      China.
FAU - Wu, Shihai
AU  - Wu S
AD  - Department of Radiation Oncology, Shenzhen People's Hospital, The Second Clinical 
      Medical College of Jinan University, The First Affiliated Hospital of Southern 
      University of Science and Technology, Shenzhen, Guangdong 518020, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20210923
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
RIN - Oncol Lett. 2023 Nov 13;27(1):15. PMID: 38028178
PMC - PMC8477075
OTO - NOTNLM
OT  - LSCC
OT  - NEAT1
OT  - SEMA4B
OT  - invasion
OT  - miR-204-5p
OT  - proliferation
COIS- The authors declare that they have no competing interests.
EDAT- 2021/10/12 06:00
MHDA- 2021/10/12 06:01
PMCR- 2021/09/23
CRDT- 2021/10/11 05:58
PHST- 2020/09/06 00:00 [received]
PHST- 2021/06/11 00:00 [accepted]
PHST- 2021/10/11 05:58 [entrez]
PHST- 2021/10/12 06:00 [pubmed]
PHST- 2021/10/12 06:01 [medline]
PHST- 2021/09/23 00:00 [pmc-release]
AID - OL-0-0-13063 [pii]
AID - 10.3892/ol.2021.13063 [doi]
PST - ppublish
SO  - Oncol Lett. 2021 Nov;22(5):802. doi: 10.3892/ol.2021.13063. Epub 2021 Sep 23.