Evidence map›Paper›PMID 28369091›Full record

ArticlePloS one2017

Knocking-down of CREPT prohibits the progression of oral squamous cell carcinoma and suppresses cyclin D1 and c-Myc expression.

Juntao Ma, Yipeng Ren, Lei Zhang, Xiangpan Kong, Tong Wang, Yueyi Shi, Rongfa Bu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Roles of Wnt ligands and receptors in oral squamous cell carcinoma.Journal of Zhejiang University. Science. B · 2025
    Review
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  6. An Important Role for RPRD1B in the Heat Shock Response.Molecular and cellular biology · 2022
    Article
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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

7 authors at 4 institutions in 1 country.

Juntao MaDepartment of Stomatology, Chinese PLA General Hospital, Beijing, China.
Yipeng RenDepartment of Stomatology, Chinese PLA General Hospital, Beijing, China.
Lei ZhangDepartment of Stomatology, Chinese PLA General Hospital, Beijing, China.
Xiangpan KongDepartment of Oral and Maxillofacial-Head and Neck Surgery, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
Tong WangSchool of Medicine, Nankai University, Tianjin, China.
Yueyi ShiDepartment of Stomatology, Chinese PLA General Hospital, Beijing, China.
Rongfa BuDepartment of Stomatology, Chinese PLA General Hospital, Beijing, China.
Chinese PLA General Hospital · CNCapital Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs a regulator essential for many cell cycle-related proteins, the robust expression of Cell cycle-Related and Expression-elevated Protein in Tumor (CREPT) implicates a poor diagnosis of endoderm and mesoderm-derived tumors. Whether CREPT plays the same role in the tumorigenesis derived from ectodermal tissues remains elusive.

methodsTo explore the role of CREPT in ectoderm-derived tumors, cells from 7oral squamous cell carcinoma (OSCC) lines and 84clinical OSCC samples were exploited in this study. Quantitative PCR, Western blot assay and immunohistochemistry were applied in the evaluation of CREPT, cyclin D1 and c-Myc expression. Knocking-down of CREPT was performed by lentivirus delivering specific shRNA of CREPT. The effects of CREPT on OSCC were examined by cell proliferation, colony formation, apoptosis, cell migration and xenograft implantation experiments.

resultsCompared with human normal oral keratinocytes, OSCC cell lines showed a significantly elevated expression of CREPT in both mRNA and protein levels. Consistently, samples from OSCC patients also exhibited a noticeably stronger CREPT expression than the noncancerous samples. In contrast, knocking down of CREPT in OSCC cell lines significantly reduced proliferation, colony formation and migration as well as the expression of cyclin D1 and c-Myc, but promoted apoptosis. Statistical analysis also suggested that CREPT expression was significantly correlated with the T and N classification of OSCC. Furthermore, CAL27 mouse xenograft model confirmed that down-regulation of CREPT prohibited cyclin D1 and c-Myc expression, through which decreased the in vivo tumor growth, but increased the survival ratio of hosts.

conclusionIn OSCC cell lines, up-regulated CREPT expression enhanced cell proliferation, migration and cell cycle as well as promoted cyclin D1 and c-Myc expression as it did in endoderm and mesoderm-origin tumors. Our study strongly suggests that CREPT could be used as a marker for the OSCC prognosis and might work as a potential target in future OSCC therapy.

Indexed as

Genes, mycAnimalsApoptosisBiomarkers, TumorCarcinoma, Squamous CellCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationCyclin D1Disease ProgressionDown-RegulationFemaleGene ExpressionGene Knockdown TechniquesHumansBiomarkers, TumorCCND1 protein, humanCell Cycle ProteinsCyclin D1Neoplasm ProteinsRNA, MessengerRNA, NeoplasmRPRD1B protein, human

Identifiers

PMID28369091
PMCPMC5378318
OpenAlexW2604697276

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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.