Evidence map›Paper›PMID 24608427›Full record

ArticleOncogene2015

miR-506 acts as a tumor suppressor by directly targeting the hedgehog pathway transcription factor Gli3 in human cervical cancer.

S-Y Wen, Y Lin, Y-Q Yu, S-J Cao, R Zhang, X-M Yang, J Li, Y-L Zhang, Y-H Wang, M-Z Ma and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 154 citations in OpenAlex.

  1. Review
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  14. Roles of Antimicrobial Peptides in Gynecological Cancers.International journal of molecular sciences · 2022
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  19. PRKCI Mediates RadiosensitivityFrontiers in oncology · 2022
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  20. Article

32 more citing papers are in PubMed but not listed here.

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 8 institutions in 1 country.

S-Y Wen1] Department of Obstetrics & Gynecology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, PR China [2] Department of Obstetrics & Gynecology, International Peace Maternity & Child Health Hospital of the China Welfare Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China [3] State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Y LinDepartment of Obstetrics & Gynecology, International Peace Maternity & Child Health Hospital of the China Welfare Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Y-Q YuDepartment of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, PR China.
S-J CaoDepartment of Obstetrics and Gynecology, Shanghai Songjiang District Central Hospital, Shanghai, PR China.
R ZhangDepartment of Obstetrics and Gynecology, Shanghai Fengxian District Central Hospital, Shanghai, PR China.
X-M YangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
J LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Y-L ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Y-H WangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
M-Z MaState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
W-W SunDepartment of Obstetrics and Gynecology, Shanghai Songjiang District Central Hospital, Shanghai, PR China.
X-L LouDepartment of Obstetrics and Gynecology, Shanghai Songjiang District Central Hospital, Shanghai, PR China.
J-H WangDepartment of Obstetrics and Gynecology, Southern Medical University, Guangzhou, PR China.
Y-C TengDepartment of Obstetrics & Gynecology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, PR China.
Z-G ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Shanghai Jiao Tong University · CNSongjiang District Central Hospital · CNState Key Laboratory of Oncogene and Related Genes · CNChina Medical University · CNShanghai Cancer Institute · CNShanghai Sixth People's Hospital · CNSouthern Medical University · CNXian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although significant advances have recently been made in the diagnosis and treatment of cervical carcinoma, the long-term survival rate for advanced cervical cancer remains low. Therefore, an urgent need exists to both uncover the molecular mechanisms and identify potential therapeutic targets for the treatment of cervical cancer. MicroRNAs (miRNAs) have important roles in cancer progression and could be used as either potential therapeutic agents or targets. miR-506 is a component of an X chromosome-linked miRNA cluster. The biological functions of miR-506 have not been well established. In this study, we found that miR-506 expression was downregulated in approximately 80% of the cervical cancer samples examined and inversely correlated with the expression of Ki-67, a marker of cell proliferation. Gain-of-function and loss-of-function studies in human cervical cancer, Caski and SiHa cells, demonstrated that miR-506 acts as a tumor suppressor by inhibiting cervical cancer growth in vitro and in vivo. Further studies showed that miR-506 induced cell cycle arrest at the G1/S transition, and enhanced apoptosis and chemosensitivity of cervical cancer cell. We subsequently identified Gli3, a hedgehog pathway transcription factor, as a direct target of miR-506 in cervical cancer. Furthermore, Gli3 silencing recapitulated the effects of miR-506, and reintroduction of Gli3 abrogated miR-506-induced cell growth arrest and apoptosis. Taken together, we conclude that miR-506 exerts its anti-proliferative function by directly targeting Gli3. This newly identified miR-506/Gli3 axis provides further insight into the pathogenesis of cervical cancer and indicates a potential novel therapeutic agent for the treatment of cervical cancer.

Indexed as

Genes, Tumor SuppressorAnimalsCell Line, TumorFemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansKi-67 AntigenKruppel-Like Transcription FactorsMiceMicroRNAsNerve Tissue ProteinsSignal TransductionUterine Cervical NeoplasmsXenograft Model Antitumor AssaysZinc Finger Protein Gli3GLI3 protein, humanKi-67 AntigenKruppel-Like Transcription FactorsMicroRNAsMIRN506 microRNA, humanNerve Tissue ProteinsZinc Finger Protein Gli3

Identifiers

PMID24608427
OpenAlexW1997153505

What OpenQuestion holds

Textmetadata
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.