Evidence map›Paper›PMID 25635878›Full record

ArticlePloS one2015

INMAP overexpression inhibits cell proliferation, induces genomic instability and functions through p53/p21 pathways.

Yan Zhu, Yan Lei, Baochen Du, Yanbo Zheng, Xiangfeng Lu, Tan Tan, Jingting Kang, Le Sun, Qianjin Liang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

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 4 institutions in 1 country.

Yan ZhuBeijing Key Laboratory of Gene Resource and Molecular Development, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China; Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China.
Yan LeiKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China.
Baochen DuBeijing Key Laboratory of Gene Resource and Molecular Development, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China.
Yanbo ZhengThe Institute of Medical Biotechnology (IMB) of the Chinese Academy of Medical Sciences, Beijing, 100050, P. R. China.
Xiangfeng LuDongzhimen Hospital of Beijing University of Chinese Traditional Medicine, Beijing, 100700, P. R. China.
Tan TanBeijing Key Laboratory of Gene Resource and Molecular Development, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China.
Jingting KangKey Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China.
Le SunAbMax Biotechnology Co., Haidian, Beijing, 100085, P. R. China.
Qianjin LiangBeijing Key Laboratory of Gene Resource and Molecular Development, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China; Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, 100875, P. R. China.
Beijing Normal University · CNAbMax AntibodyChina (China) · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNDongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

INMAP is a spindle protein that plays essential role for mitosis, by ensuring spindle and centromere integrality. The aim of this study was to investigate the relevant functions of INMAP for genomic stability and its functional pathway. We overexpressed INMAP in HeLa cells, resulting in growth inhibition in monolayer cell cultures, anchorage-independent growth in soft agar and xenograft growth in nude mice. In this system caused micronuclei (MNi) formation, chromosome distortion and γH2AX expression upregulation, suggesting DNA damage induction and genomic stability impairment. As a tumour biochemical marker, lactate dehydrogenase (LDH) isoenzymes were detected to evaluate cell metabolic activity, the results confirming that total activity of LDH, as well as that of its LDH5 isoform, is significantly decreased in INMAP-overexpressing HeLa cells. The levels of p53 and p21 were upregulated, and however, that of PCNA and Bcl-2, downregulated. Indirect immunofluorescence (IIF) and coimmunoprecipitation (CoIP) analyses revealed the interaction between INMAP and p21. These results suggest that INMAP might function through p53/p21 pathways.

Indexed as

AnimalsCell Cycle ProteinsCell ProliferationCyclin-Dependent Kinase Inhibitor p21Gene Expression RegulationGenomic InstabilityHeLa CellsHistonesHumansMiceNuclear ProteinsSignal TransductionSpindle ApparatusTumor Suppressor Protein p53Xenograft Model Antitumor AssaysCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21H2AX protein, humanHistonesINMAP protein, humanNuclear ProteinsTumor Suppressor Protein p53

Identifiers

PMID25635878
PMCPMC4312054
OpenAlexW2019422964

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.