Evidence map›Paper›PMID 36270987›Full record

ArticleCell death discovery2022

Antisense lncRNA NNT-AS1 promoted esophageal squamous cell carcinoma progression by regulating its sense gene NNT expression.

Xianglong Pan, Qi Wang, Yue Yu, Weibing Wu, Liang Chen, Wei Wang, Zhihua Li

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Mechanism of LncRNA Gm2044 in germ cell development.Frontiers in cell and developmental biology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Xianglong Pan *Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qi Wang *Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0002-3035-5887
Yue YuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Weibing WuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Liang ChenDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wei WangDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. wangwei15261883958@163.com.ORCID http://orcid.org/0000-0002-1614-0759
Zhihua LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. lizhihua_njmu@126.com.ORCID http://orcid.org/0000-0003-4820-4603
Jiangsu Province Hospital · CN

Funding

Ministry of Health of China | Wu Jieping Medical Foundation 320.6750.2020-15-8
6 · The paper itself

Abstract

Antisense lncRNAs were endogenous productions from the antisense strand of coding genes and were transcribed in the reverse direction of the sense gene. The purpose of this study was to evaluate the roles and functions of antisense lncRNAs in esophageal squamous cell carcinoma (ESCC). Differentially expressed antisense lncRNAs were initially screened based on transcriptome data of 119 paired ESCC samples in GSE53624 and were further validated in 6 paired ESCC samples from our institution. Log-rank test was adopted to identify ESCC prognosis-associated lncRNAs. Finally, functional assays were performed to reveal the functions of our identified antisense lncRNAs. In total, 174 antisense lncRNAs were differentially expressed in both GSE53624 and JSPH databases. Five of them were significantly associated with ESCC prognosis (NNT-AS1, NKILA, CCDC18-AS1, SLCO4A1-AS1, and AC110619.1). Of note, NNT-AS1 showed the most significant association with ESCC prognosis. The upregulation of NNT-AS1 was further confirmed in ESCC cells. Knockdown of NNT-AS1 inhibited ESCC cell proliferation, migration, promoted ESCC cells apoptosis, and induced cell cycle arrest in the G2/M stage. NNT-AS1 expression significantly correlated with its sense gene NNT. As expected, NNT-AS1 knockdown suppressed NNT expression. Inhibition of NNT repressed ESCC cell proliferation and migration, and accelerated ESCC cell apoptosis. Overexpression of NNT could rescue the suppressed proliferation and migration of ESCC cells induced by the silencing of NNT-AS1. In terms of mechanism, NNT-AS1 served as a competing endogenous RNA to sponge the miR-382-5p, which could inhibit NNT expression. Pathway enrichment analysis and western blot assay indicated that NNT-AS1 and NNT could regulate the cell cycle pathway. In conclusion, antisense lncRNA NNT-AS1 facilitated ECSS progression by targeting its sense gene NNT through sponging miR-382-5p. This study provided us with a deeper insight into the roles of antisense lncRNAs in ESCC and identified novel potential therapeutic targets.

Identifiers

PMID36270987
PMCPMC9586939
OpenAlexW4306980400

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.