Evidence map›Paper›PMID 28410216›Full record

ArticleOncotarget2017

Friend leukemia virus integration 1 promotes tumorigenesis of small cell lung cancer cells by activating the miR-17-92 pathway.

Lingyu Li, Wei Song, Xu Yan, Ailing Li, Xiaoying Zhang, Wei Li, Xue Wen, Lei Zhou, Dehai Yu, Ji-Fan Hu and 1 more

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. International journal of molecular medicine · 2026
    Article
  2. Role of circular RNAs in lung cancer.Frontiers in genetics · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
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

11 authors.

Lingyu LiCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Wei SongCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Xu YanCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Ailing LiStanford University Medical School, Palo Alto Veterans Institute for Research, Palo Alto, CA, USA.
Xiaoying ZhangCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Wei LiCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Xue WenCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Lei ZhouCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Dehai YuCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Ji-Fan HuCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.
Jiuwei CuiCancer Center, The First Bethune Hospital of Jilin University, Changchun, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is regarded as the most devastative type of human lung malignancies. The rapid and disseminated growth pattern remains the primary cause of poor clinical prognosis in patients with SCLC. However, the molecular factors that drive rapid progression of SCLC remain unclear. Friend leukemia virus integration 1 (FLI1), an Ets transcription factor family member, has been previously reported to act as a major driver of hematological malignancies. In this study, we explored the potential role of FLI1 in SCLC. Using immunohistochemical staining, we found that FLI1 was significantly upregulated in SCLC tissues, compared to that in non-small cell lung cancer (NSCLC) and normal lung tissues (p < 0.01). The expression score of FLI1 oncoprotein was associated with the extensive stage of SCLC and the overexpressed Ki67. Knockdown of FLI1 with small interfering RNA (siRNA) or short hairpin RNA (shRNA) promoted apoptosis and induced repression of cell proliferation, tumor colony formation and in vivo tumorigenicity in highly aggressive SCLC cell lines. Importantly, we discovered that FLI1 promoted tumorigenesis by activating the miR-17-92 cluster family. This study uncovers FLI1 as an important driving factor that promotes tumor growth in SCLC through the miR-17-92 pathway. FLI1 may serve as an attractive target for therapeutic intervention of SCLC.

Indexed as

AdultAgedApoptosisBiomarkersCell Line, TumorCell ProliferationCell Transformation, NeoplasticFemaleGene Knockdown TechniquesHumansLung NeoplasmsMaleMicroRNAsMiddle AgedMultigene FamilyNeoplasm StagingBiomarkersFLI1 protein, humanMicroRNAsProto-Oncogene Protein c-fli-1apoptosisFLI1lung cancermiR-17-92tumor

Identifiers

PMID28410216
PMCPMC5522042

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.