Evidence map›Paper›PMID 17846787›Full record

ArticleJournal of cancer research and clinical oncology2008

SCC-112 gene is involved in tumor progression and promotes the cell proliferation in G2/M phase.

M Z Zheng, L M Zheng, Y X Zeng

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. PDS5A and PDS5B in Cohesin Function and Human Disease.International journal of molecular sciences · 2021
    Review
  3. Enhanced Expression of Fibroblast Growth Factor Receptor 3 IIIc Promotes Human Esophageal Carcinoma Cell Proliferation.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016
    Article
  4. Article
  5. Article
  6. Article
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

3 authors at 2 institutions in 1 country.

M Z ZhengState Key Laboratory of Oncology in Southern China, Department of Experimental Research, Sun Yat-sen University Cancer Center, 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
L M Zheng
Y X Zeng
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSCC-112 is a novel cell cycle-related gene and differentially expressed in cancers. Suggesting the complex role of SCC-112 might be existent in cell proliferation and tumor development. The relative research on SCC-112 has been few so far. This study is attempted to explore the role of SCC-112 in tumorigenesis. EXPERIMENTAL

designRT-PCR and western blot were performed on seven tumor-normal paired tissues and nine cell lines. Immunohistochemistry was carried out for analyzing the expression of SCC-112 in nasopharyngeal tissues. 293T and three nasopharyngeal cell lines were transfected with expression vector (pCMV-SPORT6-SCC-112) or its siRNA. Cell proliferation was examined by MTT and clone formation experiments. Immunoprecipitation determined the interacted protein of SCC-112, and FACS detected cell cycle parameter on cells treated with synchronized reagent.

resultsSCC-112 ( approximately 150 kDa) is up-regulated in tumor tissue as compared to the corresponding normal tissue and was detected in the tested cell lines. Overexpression of SCC-112 ( approximately 150 kDa) in 293T and three nasopharyngeal cell lines promoted cell proliferation and clone formation while downregulation of SCC-112 ( approximately 150 kDa) in these cells resulted in the opposite. Moreover, SCC-112 was found to interact with p63 and overexpression of SCC-112 up-regulated p63 expression. SCC-112 expression level positively correlated with cells in G2/M phase.

conclusionsThese findings suggest that SCC-112 improve cell proliferation and contributes to tumorigenesis by interacting with p63 and promoting cell cycling. SCC-112 might be an alternative target in tumor biomarking and mechanistic investigation.

Indexed as

Cell DivisionG2 PhaseCell ProliferationCells, CulturedDisease ProgressionDNA-Binding ProteinsHumansImmunohistochemistryNeoplasmsNuclear ProteinsTrans-ActivatorsTranscription FactorsTumor Suppressor ProteinsDNA-Binding ProteinsNuclear ProteinsPDS5A protein, humanTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID17846787
PMCPMC12161633
OpenAlexW2169585556

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.