Evidence map›Paper›PMID 27821801›Full record

ArticleOncotarget2016

TRIM71 suppresses tumorigenesis via modulation of Lin28B-let-7-HMGA2 signaling.

Jinlong Yin, Tae-Hoon Kim, Nayun Park, Daye Shin, Hae In Choi, Sungchan Cho, Jong Bae Park, Jong Heon Kim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. RNA-Binding Protein Trim71 Controls Epicardial Cell Migration.Journal of cardiovascular development and disease · 2026
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  13. Microorganisms · 2021
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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 2 institutions in 1 country.

Jinlong YinDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, Korea.
Tae-Hoon KimSpecific Organs Cancer Branch, Research Institute, National Cancer Center, Goyang, Gyeonggi, Korea.
Nayun ParkDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, Korea.
Daye ShinDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, Korea.
Hae In ChoiDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, Korea.
Sungchan ChoAnticancer Agent Research Center, Korea Research Institute of Bioscience & Biotechnology, Ochang, Korea.
Jong Bae ParkDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, Korea.
Jong Heon KimDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, Korea.
National Cancer Center · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TRIM71 (tripartite motif-containing 71) belongs to the TRIM-NHL protein family, which plays a conserved role in regulating early development and differentiation. However, the molecular functions of TRIM71 have remained largely unknown. Here, we explored the role of TRIM71 together with modulation of Lin28B-let-7-HMGA2 (high-mobility group AT-hook 2) signaling in tumorigenesis. TRIM71 overexpression opposed Lin28B-induced transformation in primary cells and inhibited tumor formation in a mouse model. Specific knockdown of TRIM71 expression increased cancer cell proliferation and invasion. Conversely, overexpression of wild-type TRIM71 in non-small cell lung carcinoma (NSCLC) cells in which Lin28B-let-7-HMGA2 signaling was conserved decreased both cancer cell phenotypes. More importantly, overexpression of an ubiquitin transfer activity-deficient TRIM71 mutant in NSCLC cells had no effect on proliferation or invasion, regardless of the conservation status of Lin28B-let-7-HMGA2 signaling. The tumorigenic inhibitory action of TRIM71 was antagonized by overexpression of the TRIM71 downstream targets, Lin28B and HMGA2. Furthermore, a bioinformatics analysis revealed that TRIM71 expression was downregulated in various types of cancer tissue from patients. Taken together, these data indicate that TRIM71 acts through post-transcriptional repression of Lin28B and subsequent modulation of let-7-HMGA2 signaling during tumorigenesis to potentially function as a tumor suppressor.

Indexed as

AnimalsCaco-2 CellsCarcinogenesisCells, CulturedFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHEK293 CellsHMGA2 ProteinHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsNIH 3T3 CellsRNA-Binding ProteinsHMGA2 ProteinLIN28B protein, humanMicroRNAsmirnlet7 microRNA, humanRNA-Binding ProteinsTRIM71 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesHMGA2let-7Lin28BTRIM71tumorigenesis

Identifiers

PMID27821801
PMCPMC5346756
OpenAlexW2548615291

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.