Evidence map›Paper›PMID 26170120›Full record

ArticleBMC genetics2015

Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region.

Carola Hedberg Oldfors, Diego Garcia Dios, Anna Linder, Kittichate Visuttijai, Emma Samuelson, Sandra Karlsson, Staffan Nilsson, Afrouz Behboudi

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

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  14. miR-137 plays tumor suppressor roles in gastric cancer cell lines by targeting KLF12 and MYO1C.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

8 authors at 3 institutions in 1 country.

Carola Hedberg OldforsDepartment of Medical and Clinical Genetics, Sahlgrenska Academy, University of Gothenburg, SE-40530, Gothenburg, Sweden. carola.oldfors@gu.se.
Diego Garcia DiosDepartment of Medical and Clinical Genetics, Sahlgrenska Academy, University of Gothenburg, SE-40530, Gothenburg, Sweden. dagarciadios@gmail.com.
Anna LinderDepartment of Medical and Clinical Genetics, Sahlgrenska Academy, University of Gothenburg, SE-40530, Gothenburg, Sweden. anna.linder@gu.se.
Kittichate VisuttijaiDepartment of Medical and Clinical Genetics, Sahlgrenska Academy, University of Gothenburg, SE-40530, Gothenburg, Sweden. kittichate.visuttijai@his.se.
Emma SamuelsonDepartment of Medical and Clinical Genetics, Sahlgrenska Academy, University of Gothenburg, SE-40530, Gothenburg, Sweden. emma.samuelson@gu.se.
Sandra KarlssonTumor Biology Research Group, School of Bioscience, University of Skövde, SE-54128, Skövde, Sweden. sandra.karlsson@his.se.
Staffan NilssonInstitute of Mathematical Statistics, Chalmers University of Technology, SE-41296, Gothenburg, Sweden. steffan.nilsson@chalmers.se.
Afrouz BehboudiTumor Biology Research Group, School of Bioscience, University of Skövde, SE-54128, Skövde, Sweden. afrouz.behboudi@his.se.
University of Gothenburg · SEUniversity of Skövde · SEChalmers University of Technology · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral reports indicate a commonly deleted chromosomal region independent from, and distal to the TP53 locus in a variety of human tumors. In a previous study, we reported a similar finding in a rat tumor model for endometrial carcinoma (EC) and through developing a deletion map, narrowed the candidate region to 700 kb, harboring 19 genes. In the present work real-time qPCR analysis, Western blot, semi-quantitative qPCR, sequencing, promoter methylation analysis, and epigenetic gene expression restoration analyses (5-aza-2'-deoxycytidine and/or trichostatin A treatments) were used to analyze the 19 genes located within the candidate region in a panel of experimental tumors compared to control samples.

resultsReal-time qPCR analysis suggested Hic1 (hypermethylated in cancer 1), Inpp5k (inositol polyphosphate-5-phosphatase K; a.k.a. Skip, skeletal muscle and kidney enriched inositol phosphatase) and Myo1c (myosin 1c) as the best targets for the observed deletions. No mutation in coding sequences of these genes was detected, hence the observed low expression levels suggest a haploinsufficient mode of function for these potential tumor suppressor genes. Both Inpp5k and Myo1c were down regulated at mRNA and/or protein levels, which could be rescued in gene expression restoration assays. This could not be shown for Hic1.

conclusionInnp5k and Myo1c were identified as the best targets for the deletions in the region. INPP5K and MYO1C are located adjacent to each other within the reported independent region of tumor suppressor activity located at chromosome arm 17p distal to TP53 in human tumors. There is no earlier report on the potential tumor suppressor activity of INPP5K and MYO1C, however, overlapping roles in phosphoinositide (PI) 3-kinase/Akt signaling, known to be vital for the cell growth and survival, are reported for both. Moreover, there are reports on tumor suppressor activity of other members of the gene families that INPP5K and MYO1C belong to. Functional significance of these two candidate tumor suppressor genes in cancerogenesis pathways remains to be investigated.

Indexed as

Genes, Tumor SuppressorGenetic LociAnimalsAzacitidineDNA MethylationFemaleGene Expression RegulationHumansHydroxamic AcidsInositol Polyphosphate 5-PhosphatasesMyosin Type IPhosphoric Monoester HydrolasesRatsTumor Suppressor Protein p53AzacitidineHydroxamic AcidsInositol Polyphosphate 5-PhosphatasesMYO1C protein, humanMyosin Type IPhosphoric Monoester Hydrolasestrichostatin ATumor Suppressor Protein p53

Identifiers

PMID26170120
PMCPMC4501283
OpenAlexW1640900830

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.