Evidence map›Paper›PMID 25526032›Full record

ArticleOncotarget2014

DNA mismatch repair gene MLH1 induces apoptosis in prostate cancer cells.

Shinichiro Fukuhara, Inik Chang, Yozo Mitsui, Takeshi Chiyomaru, Soichiro Yamamura, Shahana Majid, Sharanjot Saini, Hiroshi Hirata, Guoren Deng, Ankurpreet Gill and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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

15 authors at 5 institutions in 3 countries.

Shinichiro FukuharaDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America. Department of Urology, Osaka University Graduate School of Medicine, Suita, Japan.
Inik ChangDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Oral Biology,Yonsei University College of Dentistry, Seoul, Korea.
Yozo MitsuiDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America. Department of Urology, Shimane University Faculty of Medicine, Izumo, Japan.
Takeshi ChiyomaruDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America. Department of Urology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Soichiro YamamuraDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
Shahana MajidDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
Sharanjot SainiDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
Hiroshi HirataDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
Guoren DengDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
Ankurpreet GillDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America.
Darryn K WongDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America.
Hiroaki ShiinaDepartment of Urology, Shimane University Faculty of Medicine, Izumo, Japan.
Norio NonomuraDepartment of Urology, Osaka University Graduate School of Medicine, Suita, Japan.
Rajvir DahiyaDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
Yuichiro TanakaDepartment of Surgery/Urology, Veterans Affairs Medical Center, San Francisco, California, United States of America. Department of Urology, University of California, San Francisco, California, United States of America.
San Francisco VA Medical Center · USUniversity of California, San Francisco · USOsaka University · JPShimane University · JPYonsei University · KR

Funding

DNA methylation in aging, race and prostate cancerR01AG021418 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI DAHIYA, RAJVIR · 2002 to 2006
$1.6M
Role of genetic biomarkers in clinical assessment of prostate cancerIP1BX001604 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI DAHIYA, RAJVIR, LAU, YUN-FAI CHRIS · 2013 to 2016
–
BLRD VA I01 BX001123BLRD VA IP1 BX001604NIA NIH HHS R01 AG021418
6 · The paper itself

Abstract

Mismatch repair (MMR) enzymes have been shown to be deficient in prostate cancer (PCa). MMR can influence the regulation of tumor development in various cancers but their role on PCa has not been investigated. The aim of the present study was to determine the functional effects of the mutL-homolog 1 (MLH1) gene on growth of PCa cells. The DU145 cell line has been established as MLH1-deficient and thus, this cell line was utilized to determine effects of MLH1 by gene expression. Lack of MLH1 protein expression was confirmed by Western blotting in DU145 cells whereas levels were high in normal PWR-1E and RWPE-1 prostatic cells. MLH1-expressing stable transfectant DU145 cells were then created to characterize the effects this MMR gene has on various growth properties. Expression of MLH1 resulted in decreased cell proliferation, migration and invasion properties. Lack of cell growth in vivo also indicated a tumor suppressive effect by MLH1. Interestingly, MLH1 caused an increase in apoptosis along with phosphorylated c-Abl, and treatment with MLH1 siRNAs countered this effect. Furthermore, inhibition of c-Abl with STI571 also abrogated the effect on apoptosis caused by MLH1. These results demonstrate MLH1 protects against PCa development by inducing c-Abl-mediated apoptosis.

Indexed as

DNA Mismatch RepairAdaptor Proteins, Signal TransducingAnimalsApoptosisBenzamidesCell Line, TumorHeterograftsHumansImatinib MesylateMaleMiceMice, NudeMutL Protein Homolog 1Nuclear ProteinsPhosphorylationPiperazinesAdaptor Proteins, Signal TransducingBenzamidesImatinib MesylateMLH1 protein, humanMutL Protein Homolog 1Nuclear ProteinsPiperazinesProtein Kinase InhibitorsProto-Oncogene Proteins c-ablPyrimidines

Identifiers

PMID25526032
PMCPMC4294331
OpenAlexW2146706493

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.