Evidence map›Paper›PMID 27347311›Full record

ArticleAmerican journal of translational research2016

Up-regulation of long non-coding HOTTIP functions as an oncogene by regulating HOXA13 in non-small cell lung cancer.

Yulan Sang, Fucheng Zhou, Dongjie Wang, Xin Bi, Xuanxi Liu, Zhen Hao, Qingsong Li, Wei Zhang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
4.7field-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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  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

8 authors at 1 institution in 1 country.

Yulan SangDepartment of Respiratory, The First Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Fucheng ZhouDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Dongjie WangDepartment of Respiratory, The First Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Xin BiDepartment of Respiratory, The First Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Xuanxi LiuDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Zhen HaoDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Qingsong LiDepartment of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Wei ZhangDepartment of Respiratory, The First Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is the major cause of cancer death worldwide. Increasing evidences show that long non coding RNAs (lncRNAs) are widely involved in the development and progression of NSCLC. The lncRNA HOTTIP has been identified as an oncogene in several human cancers, but its role in NSCLC remains unknown. The present study was to determine the expression and function of HOTTIP in NSCLC. Quantitative real-time PCR was used to detect the expressions of HOTTIP in 53 paired NSCLC tissues and cell lines. Furthermore, RNA interference (RNAi) and over-expression approaches were used to investigate the biological function of HOTTIP in lung cancer cell line. The impacts of HOTTIP on cell migration, proliferation and apoptosis were analyzed using wound scratch assay, MTT and flow cytometry, respectively. The results revealed that the HOTTIP expression was significantly up-regulated in NSCLC tissues and cells when compared with corresponding adjacent normal tissues and normal bronchial epithelial cells (p<0.05). Furthermore, knock-down of HOTTIP significantly inhibited cell proliferation, migration and induced cell apoptosis in vitro, while over-expression of HOTTIP led to the opposite effects. In addition, we identified HOTTIP as a transcriptional regulator of HOXA13 in lung cancer cell. Ectopic expression of HOTTIP suppressed the endogenous level of HOXA13, while knock-down of HOTTIP increased HOXA13 expression. Knock-down of HOXA13 by RNA interference (siHOXA13) revealed that HOTTIP promoted lung cell proliferation, migration, and inhibited apoptosis, at least partly by regulating HOXA13. The present study is the first to identify that HOTTIP functions as an oncogene by regulating HOXA13 in NSCLC, which may represent a new biomarker and a potential therapeutic target for NSCLC intervention.

Indexed as

HOTTIPHOXA13NSCLConcogene

Identifiers

PMID27347311
PMCPMC4891416
OpenAlexW2473446026

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.