Evidence map›Paper›PMID 27829234›Full record

ArticleOncotarget2016

A regulatory loop involving miR-29c and Sp1 elevates the TGF-β1 mediated epithelial-to-mesenchymal transition in lung cancer.

Hai-Wei Zhang, En-Wen Wang, Li-Xian Li, Shou-Hui Yi, Lu-Chun Li, Fa-Liang Xu, Dong-Lin Wang, Yong-Zhong Wu, Wei-Qi Nian

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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 10% 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, 58 citations in OpenAlex.

  1. Review
  2. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  3. Review
  4. Article
  5. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
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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

9 authors at 1 institution in 1 country.

Hai-Wei ZhangKey Laboratory of Oncology, Chongqing Cancer Institute, Chongqing Cancer Hospital, Chongqing Cancer Center, Chongqing, China.
En-Wen WangDepartment of Oncology, Chongqing Cancer Institute, Chongqing, China.
Li-Xian LiKey Laboratory of Oncology, Chongqing Cancer Institute, Chongqing Cancer Hospital, Chongqing Cancer Center, Chongqing, China.
Shou-Hui YiKey Laboratory of Oncology, Chongqing Cancer Institute, Chongqing Cancer Hospital, Chongqing Cancer Center, Chongqing, China.
Lu-Chun LiDepartment of Oncology, Chongqing Cancer Institute, Chongqing, China.
Fa-Liang XuCenter of Breast Cancer, Chongqing Cancer Institute, Chongqing, China.
Dong-Lin WangDepartment of Oncology, Chongqing Cancer Institute, Chongqing, China.
Yong-Zhong WuDepartment of Radiotherapy, Chongqing Cancer Institute, Chongqing, China.
Wei-Qi NianKey Laboratory of Oncology, Chongqing Cancer Institute, Chongqing Cancer Hospital, Chongqing Cancer Center, Chongqing, China.
Chongqing Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Specificity protein1 (Sp1) is required for TGF-β-induced epithelial-to-mesenchymal transition (EMT) which has been demonstrated to aggravate the progression of cancer including lung cancer. microRNA-29c (miR-29c) is identified to inhibit EMT, but the correlation between miR-29c and Sp1 in human lung cancer remain incompletely clarified. Here, we confirmed decreased expression of miR-29c and enhanced expression of Sp1 in lung cancer tissues (n = 20) and found that Sp1 could be targeted and inhibited by miR-29c. Besides, the expression of miR-29c was down-regulated in high-metastatic lung cancer cell lines and TGF-β1-treated cells. The inhibition of miR-29c or overexpression of Sp1 in 95C and A549 cells dramatically enhanced the cell migration and invasion, and also induced the decrease in the expression of epithelial markers, e.g. thyroid transcription factor 1 (TTF-1) and E-cadherin, together with an increase in mesenchymal markers including vimentin, α-smooth muscle actin (α-SMA), which could be restored by overexpression of miR-29c mimics during the TGF-β-induced EMT. Moreover, dual-luciferase reporter assay was performed and the results indicated that miR-29c/Sp1 could form an auto-regulatory loop with TGF-β1, which impaired TGFB1 transcription. Furthermore, miR-29c overexpression could abrogate the tumor progression and inhibit the Sp1/TGF-β expressions in vivo, indicating that miR-29c could be a tumor suppressor and repress the Sp1/TGF-β axis-induced EMT in lung cancer.

Indexed as

AnimalsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansLung NeoplasmsMiceMicroRNAsNeoplasm InvasivenessSp1 Transcription FactorTransforming Growth Factor beta1MicroRNAsMIRN29a microRNA, humanSP1 protein, humanSp1 Transcription FactorTransforming Growth Factor beta1EMTmetastasismiR-29csp1TGF-β1

Identifiers

PMID27829234
PMCPMC5349884
OpenAlexW2548971289

What OpenQuestion holds

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LicenceCC BY
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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.