Evidence map›Paper›PMID 29053395›Full record

ArticleCancer biology & therapy2017

Overexpression of HN1L promotes cell malignant proliferation in non-small cell lung cancer.

Lei Li, Ting-Ting Zeng, Bao-Zhu Zhang, Yan Li, Ying-Hui Zhu, Xin-Yuan Guan

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  10. NAADP-binding proteins find their identity.Trends in biochemical sciences · 2022
    Review
  11. Review
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  13. Article
  14. Article
  15. Article
  16. Frontiers in cellular and infection microbiology · 2021
    Article
  17. Article
  18. Review
  19. 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

6 authors at 3 institutions in 2 countries.

Lei Lia State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center , Guangzhou , Guangdong , China.
Ting-Ting Zenga State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center , Guangzhou , Guangdong , China.
Bao-Zhu Zhanga State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center , Guangzhou , Guangdong , China.
Yan Lia State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center , Guangzhou , Guangdong , China.
Ying-Hui Zhua State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center , Guangzhou , Guangdong , China.
Xin-Yuan Guana State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center , Guangzhou , Guangdong , China.
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is a progressive malignant disease, involving the activation of oncogenes and inactivation of tumor suppressors. In this study, we identified and characterized a novel oncogene hematopoietic- and neurologic-expressed sequence 1-like (HN1L) in human NSCLC. Overexpression of HN1L was frequently detected in primary NSCLC compared with their non-tumor counterparts (P < 0.001), which was significantly associated with tumor size (P = 0.022). In addition, Kaplan-Meier analysis showed that upregulation of HN1L correlated with worse overall survival (P = 0.029) and disease-free survival (P = 0.011) for NSCLC patients. Both in vitro and in vivo studies demonstrated that inhibition of HN1L expression with shRNA dramatically inhibited cell growth, adherent and non-adherent colony formation, and tumorigenicity in nude mice. The positive correlation of HN1L expression and Ki67 level in a large NSCLC samples further suggested the key role of HN1L in the regulation of cell growth. Further study showed that knockdown of HN1L resulted in dramatic cell cycle arrest by interfering with MAPK pathway via interacting with RASA4 protein. In conclusion, HN1L plays a crucial role in the progression of NSCLC by contributing to malignant proliferation, with possible use as a new intervention point for therapeutic strategies.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Cycle ProteinsCell Line, TumorCell ProliferationFemaleGene Knockdown TechniquesHeterograftsHumansLung NeoplasmsMaleMiceMice, NudeMicrotubule-Associated ProteinsNerve Tissue ProteinsNuclear ProteinsCell Cycle ProteinsJPT1 protein, humanMicrotubule-Associated ProteinsNerve Tissue ProteinsNuclear ProteinsHN1LMAPK pathwayNSCLCprognosisproliferation

Identifiers

PMID29053395
PMCPMC5710669
OpenAlexW2765316976

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.