Evidence map›Paper›PMID 25120759›Full record

ArticleInternational journal of clinical and experimental pathology2014

PNMA1 promotes cell growth in human pancreatic ductal adenocarcinoma.

Shu-Heng Jiang, Ping He, Ming-Ze Ma, Yang Wang, Rong-Kun Li, Fang Fang, Ying Fu, Guang-Ang Tian, Wen-Xin Qin, Zhi-Gang Zhang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 22 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

10 authors at 4 institutions in 1 country.

Shu-Heng JiangShanghai Medical College of Fudan University Shanghai 200032, P.R. China ; State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Ping HeState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Ming-Ze MaState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Yang WangShanghai Medical College of Fudan University Shanghai 200032, P.R. China ; State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Rong-Kun LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Fang FangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Ying FuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Guang-Ang TianState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Wen-Xin QinShanghai Medical College of Fudan University Shanghai 200032, P.R. China ; State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Zhi-Gang ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200240, P.R. China.
Renji Hospital · CNShanghai Cancer Institute · CNShanghai Jiao Tong University · CNState Key Laboratory of Oncogene and Related Genes · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paraneoplastic Ma1 (PNMA1) is a member of an expanding family of 'brain/testis' proteins involved in an autoimmune disorder defined as paraneoplastic neurological syndrome (PNS). Although it is widely studied in PNS, little is known about the underlying clinical significance and biological function of PNMA1 in tumors. Here, we find that elevated PNMA1 expression is more commonly observed in pancreatic ductal adenocarcinoma (PDAC) cell lines, compared with normal pancreatic cell and tissues from pancreatic ductal adenocarcinoma patient. Besides, higher PNMA1 expression is closely correlated with large tumor size. Suppression of endogenous PNMA1 expression decreases cell viability and promotes cell apoptosis. Subsequent studies reveal that the PI3K/AKT, MAPK/ERK pathway and members of the anti-apoptotic Bcl-2 family may be involved in the pro-survival and anti-apoptotic effect of PNMA1 on PDAC. Taken together, this study provides evidence that PNMA1 is involved in tumor growth of pancreatic carcinoma and PNMA1-related pathways might represent a new treatment strategy.

Indexed as

AgedAntigensBlotting, WesternCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationFemaleHumansImmunohistochemistryMaleMiddle AgedPancreatic NeoplasmsReal-Time Polymerase Chain ReactionSignal TransductionTissue Array AnalysisAntigensMa1 antigenapoptosiscell survivalgrowthpancreatic ductal adenocarcinomaPNMA1

Identifiers

PMID25120759
PMCPMC4128994
OpenAlexW2236640083

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.