Evidence map›Paper›PMID 31436388›Full record

ArticleCancer medicine2019

Long noncoding RNA PART1 promotes progression of non-small cell lung cancer cells via JAK-STAT signaling pathway.

Dengyan Zhu, Yang Yu, Wei Wang, Kai Wu, Donglei Liu, Yang Yang, Chunyang Zhang, Yu Qi, Song Zhao

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Rewiring cancer epigenome: lncRNA as modulator of chromatin architecture and neoplastic transformation.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Review
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  18. Article
  19. Long Non-coding RNAs, LncSub-cellular biochemistry · 2022
    Article
  20. Article
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

9 authors at 2 institutions in 1 country.

Dengyan ZhuDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.
Yang YuDepartment of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Wei WangDepartment of Thoracic Surgery, Henan Medical Association, Zhengzhou, China.
Kai WuDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.
Donglei LiuDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.
Yang YangDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.
Chunyang ZhangDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.
Yu QiDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.
Song ZhaoDepartment of Thoracic Surgery, The First Affiliate Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0001-7172-1209
First Affiliated Hospital of Zhengzhou University · CNChinese Medical Association · CN

Funding

Natural Science Foundation of Henan Province 182300410383
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC), the major type of lung cancer, becomes the greatest threat to the life of people. Growing evidence shows prostate androgen-regulated transcript 1 (PART1) is considered as effective markers for prostate cancer, and has been shown to be associated with poor prognosis of NSCLC. However, the tumorigenic mechanism of PART1 in NSCLC remains to be investigated. In this study, we found that the expression of PART1 was robustly induced in NSCLC tissues and cell lines. Functional studies established that overexpression of PART1 could promote NSCLC cell proliferation, migration, and invasion, while interference of PART1 inhibited NSCLC progression. Our results also identified miR-635 as a novel target of PART1, whose expression was inhibited by PART1 in NSCLC cell lines. Moreover, gain- and loss-of-function studies revealed that PART1 could sponge miR-635 and increase the expression of Janus kinase (JAK) and signal transducer and activator of transcription proteins (STATs). Finally, we deciphered the molecular mechanism by which PART1 contributed to promotion of NSCLC cell progression via phosphorylation and activation of JAK-STAT signaling pathway. The animal experiment further confirmed that interference of NSCLC could suppress in vivo tumorigenic ability of NSCLC with favorable pharmacological activity via inactivation of JAK-STAT signaling pathway. In conclusion, our findings clarified the biologic significance of PART1/miR-635/JAK-STAT axis in NSCLC progression and provided novel evidence that PART1 may be a new potential therapeutic target for the treatment of NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAgedAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleHumansJanus Kinase 1MaleMice, Inbred BALB CMice, NudeMicroRNAsPrognosisJAK1 protein, humanJanus Kinase 1MicroRNAsMIRN635 microRNA, humanPART-1 RNA, humanRNA, UntranslatedSTAT Transcription FactorsJAK-STATmiR-635NSCLCPART1progression

Identifiers

PMID31436388
PMCPMC6792487
OpenAlexW2969622467

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.