Evidence map›Paper›PMID 31558704›Full record

ArticleCell death & disease2019

microRNA-17 functions as an oncogene by downregulating Smad3 expression in hepatocellular carcinoma.

Zhufeng Lu, Xiuhua Li, Yongfeng Xu, Miaomiao Chen, Wei Chen, Tao Chen, Qinghe Tang, Zhiying He

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.7field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Identifying the roles of miR-17 in ciliogenesis and cell cycle.Frontiers in cell and developmental biology · 2024
    Article
  5. Review
  6. miR-17-5p slows progression of hepatocellular carcinoma by downregulating TGFβR2.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Zhufeng LuDepartment of Anesthesia, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China. lu.zhufeng@zs-hospital.sh.cn.
Xiuhua LiInstitute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200123, P. R. China.
Yongfeng XuLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China.
Miaomiao ChenInstitute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200123, P. R. China.
Wei ChenDepartment of Anesthesia, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China.
Tao ChenDepartment of Hepatobiliary Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 33 Ying Feng Road, Guangzhou, Guangdong, 510289, P. R. China.
Qinghe TangDepartment of Hepatobiliary and Pancreatic Surgery, Shanghai East Hospital, Tongji University, Shanghai, 200123, P. R. China. datang1978@sina.com.
Zhiying HeInstitute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200123, P. R. China. zyhe@tongji.edu.cn.ORCID http://orcid.org/0000-0002-0087-2277
Shanghai East Hospital · CNSun Yat-sen University · CNFudan University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sekelsky mothers against dpp3 (Smad3) functions as a transcriptional modulator activated by transforming growth factor-β (TGF-β). Accumulated evidences indicated that Smad3 played the important roles in carcinogenesis and progression of hepatocellular carcinoma (HCC). Up to now, the regulatory mechanism of Smad3 in HCC still remains unclear. It has been known that some particular microRNAs (miRNAs) involve in carcinogenesis through the regulation of gene expressions with targeting mRNAs. In our study, the unknown candidates of miRNAs that target Smad3 mRNA were searched by using a newly established in vivo approach, the miRNA in vivo precipitation (miRIP). Using a loss-of-function assay, we demonstrated that miR-17 directly targeted Smad3 in HCC cells and inhibition on miR-17 increased Smad3 expression. Furthermore, we found that downregulation on Smad3 expression was consistent with high level of miR-17 in HCC tissues of patients when compared with around normal liver tissues. The manipulated miR-17 silence in HCC cells suppressed their growth of both in vitro and in vivo. Such suppression on cell growth could be recovered through downregulating Smad3. In addition, miR-17 affected cell proliferation through arresting cell cycle in G1 phase. The negative correlation between levels of miR-17 and protein levels of Smad3 was supported by the results of analysis with HCC tissue chip. In summary, for the first time, we confirmed that miR-17 directly targeted Smad3 mRNA and downregulated Smad3 protein expression in HCC. Our results indicated that the increased expression of miR-17 promoted carcinogenesis of HCC through down-regulations of Smad3, suggesting miR-17 might serve as the potential diagnostic and therapeutic targets for clinical HCC.

Indexed as

OncogenesAnimalsCarcinogenesisCarcinoma, HepatocellularCell ProliferationDown-RegulationFemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMaleMiceMice, Inbred NODMice, SCIDMicroRNAsMIRN17 microRNA, humanRNA, Small InterferingSmad3 ProteinSMAD3 protein, human

Identifiers

PMID31558704
PMCPMC6763424
OpenAlexW2976480830

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.