Evidence map›Paper›PMID 35816613›Full record

ArticleCancer biology & therapy2022

Fatty acid binding protein 5 promotes the proliferation, migration, and invasion of hepatocellular carcinoma cells by degradation of Krüppel-like factor 9 mediated by miR-889-5p via cAMP-response element binding protein.

Yanping Tang, Kezhi Li, Bangli Hu, Zhengmin Cai, Jilin Li, Hao Tao, Ji Cao

Open access · goldAbstract read
In one paragraph

Article in Cancer biology & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Cells · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. 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

7 authors at 1 institution in 1 country.

Yanping TangDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.
Kezhi LiDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.
Bangli HuDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.
Zhengmin CaiDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.
Jilin LiDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.
Hao TaoDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.
Ji CaoDepartment of Research, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.ORCID 0000-0003-1302-9112
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence has demonstrated that fatty acid binding protein 5 (FABP5) is commonly upregulated in many human malignancies. However, the mechanisms explaining the involvement of FABP5 in hepatocellular carcinoma (HCC) remain unclear. In this study, we demonstrated the involvement of FABP5 and its downstream signaling molecules in HCC progression. We first confirmed that FABP5 expression was upregulated in HCC. Additionally, FABP5 promoted HCC cells proliferation, migration, and invasion. Mechanistic investigation showed that FABP5 could improve cAMP-response element binding protein (CREB) phosphorylation. Meanwhile, CREB, as a transcription factor, upregulated the miR-889-5p expression by binding to the miR-889-5p promoter region. Consequently, miR-889-5p led to downregulation of Krüppel-like factor 9 (KLF9) by binding to the 3'-UTR of the KLF9 mRNA, potentiating the PI3K/AKT signaling pathway and promoting the proliferation, migration, and invasion of HCC cells. Our findings have identified a FABP5/CREB/miR-889-5p/KLF9 axis for HCC progression, and we postulate that blocking this key signaling pathway may represent a promising strategy for HCC treatment.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicroRNAs3' Untranslated RegionsCell Line, TumorCell MovementCell ProliferationCyclic AMP Response Element-Binding ProteinFatty Acid-Binding ProteinsGene Expression Regulation, NeoplasticHumansKruppel-Like Transcription FactorsPhosphatidylinositol 3-KinasesResponse Elements3' Untranslated RegionsCyclic AMP Response Element-Binding ProteinFABP5 protein, humanFatty Acid-Binding ProteinsKLF9 protein, humanKruppel-Like Transcription FactorsMicroRNAsPhosphatidylinositol 3-KinasescAMP-response element binding proteinFatty acid binding protein 5hepatocellular carcinomaKrüppel-like factor 9miR-889-5p

Identifiers

PMID35816613
PMCPMC9275499
OpenAlexW4285011090

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.