Evidence map›Paper›PMID 25826661›Full record

ArticleRNA biology2015

microRNA-200b and microRNA-200c promote colorectal cancer cell proliferation via targeting the reversion-inducing cysteine-rich protein with Kazal motifs.

Yi Pan, Hongwei Liang, Weixu Chen, Hongjie Zhang, Nan Wang, Feng Wang, Suyang Zhang, Yanqing Liu, Chihao Zhao, Xin Yan and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Expression of Reversion-Inducing Cysteine-Rich Protein with Kazal Motifs (International journal of molecular sciences · 2024
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  3. Article
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  5. Biomedicines · 2022
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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

15 authors at 6 institutions in 2 countries.

Yi Pana Jiangsu Engineering Research Center for microRNA Biology and Biotechnology; State Key Laboratory of Pharmaceutical Biotechnology; School of Life Sciences; Nanjing University ; Nanjing , Jiangsu , China.
Hongwei Liang
Weixu Chen
Hongjie Zhang
Nan Wang
Feng Wang
Suyang Zhang
Yanqing Liu
Chihao Zhao
Xin Yan
Junfeng Zhang
Chen-Yu Zhang
Hongwei Gu
Ke Zen
Xi Chen
Nanjing University · CNPharmaceutical Biotechnology (Czechia) · CZState Key Laboratory of Pharmaceutical BiotechnologyNanjing Drum Tower Hospital · CNJiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-200b and microRNA-200c (miR-200b/c) are 2 of the most frequently upregulated oncomiRs in colorectal cancer cells. The role of miR-200b/c during colorectal tumorigenesis, however, remains unclear. In the present study, we report that miR-200b/c can promote colorectal cancer cell proliferation via targeting the reversion-inducing cysteine-rich protein with Kazal motifs (RECK). Firstly, bioinformatics analysis predicted RECK as a conserved target of miR-200b/c. By overexpressing or knocking down miR-200b/c in colorectal cancer cells, we experimentally validated that miR-200b/c are direct regulators of RECK. Secondly, an inverse correlation between the levels of miR-200b/c and RECK protein was found in human colorectal cancer tissues and cell lines. Thirdly, we demonstrated that repression of RECK by miR-200b/c consequently triggered SKP2 (S-phase kinase-associated protein 2) elevation and p27(Kip1) (also known as cyclin-dependent kinase inhibitor 1B) degradation in colorectal cancer cells, which eventually promotes cancer cell proliferation. Finally, promoting tumor cell growth by miR-200b/c-targeting RECK was also observed in the xenograft mouse model. Taken together, our results demonstrate that miR-200b/c play a critical role in promoting colorectal tumorigenesis through inhibiting RECK expression and subsequently triggering SKP2 elevation and p27(Kip1) degradation.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCaco-2 CellsCarcinogenesisCell ProliferationColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p27GPI-Linked ProteinsHT29 CellsHumansMiceMicroRNAsNeoplasm TransplantationRNA, Small InterferingSignal TransductionS-Phase Kinase-Associated ProteinsCyclin-Dependent Kinase Inhibitor p27GPI-Linked ProteinsMicroRNAsMIRN200 microRNA, humanRECK protein, humanRNA, Small InterferingS-Phase Kinase-Associated Proteins3′-UTR, 3′-untranslated regionCDKN1B, cyclin-dependent kinase inhibitor 1Bcell proliferationcolorectal cancerCRC, colorectal cancerEdU, 5-ethynyl-2′-deoxyuridineEMT, epithelial-mesenchymal transitionmiR-200b/cmiR-200b/c, microRNA-200b and microRNA-200cmiRNA, microRNAMMP, metalloproteinaseNAT, normal adjacent tissueoncogeneORF, open reading frameRECKRECK, reversion-inducing cysteinerich protein with Kazal motifssiRNA, small interfering RNASKP2, S-phase kinase-associated protein 2ZEB, zinc finger E-box-binding protein

Identifiers

PMID25826661
PMCPMC4615722
OpenAlexW2158362045

What OpenQuestion holds

Textmetadata
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.