Evidence map›Paper›PMID 34099637›Full record

ArticleCell death & disease2021

TRPM2 promotes pancreatic cancer by PKC/MAPK pathway.

Rui Lin, Xunxia Bao, Hui Wang, Sibo Zhu, Zhongyan Liu, Quanning Chen, Kaixing Ai, Baomin Shi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 69 citations in OpenAlex.

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  15. The function of chloride channels in digestive system disease (Review).International journal of molecular medicine · 2025
    Review
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  20. Design and synthesis of 3,4-Frontiers in chemistry · 2025
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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.

Rui LinGeneral Surgery Department, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. blackchimney@tongji.edu.cn.ORCID 0000-0002-3197-9798
Xunxia BaoSchool of Life Science, Anhui Medical University, Hefei, 230022, China.ORCID 0000-0002-6085-7319
Hui WangGeneral Surgery Department, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Sibo ZhuSchool of Life Sciences, Fudan University, Shanghai, 200438, China.ORCID 0000-0003-4800-8987
Zhongyan LiuGeneral Surgery Department, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Quanning ChenGeneral Surgery Department, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Kaixing AiShanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, 200082, China.
Baomin ShiGeneral Surgery Department, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. baominsph@163.com.ORCID 0000-0001-8791-569X
Tongji University · CNAnhui Medical University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism of pancreatic cancer (PA) is not fully understanded. In our last report, TRPM2 plays a promising role in pancreatic cancer. However, the mechanism of TRPM2 is still unknown in this dismal disease. This study was designed to investigate the role and mechanism of TRPM2 in pancreatic cancer. TRPM2 overexpressed and siRNA plasmid were created and transfected with pancreatic cancer cell line (BxPC-3) to construct the cell model. We employed CCK-8, Transwell, scratch wound, and nude mice tumor-bearing model to investigate the role of TRPM2 in pancreatic cancer. Besides, we collected the clinical data, tumor tissue sample (TT) and para-tumor sample (TP) from the pancreatic cancer patients treated in our hospital. We analyzed the mechanism of TRPM2 in pancreatic cancer by transcriptome analysis, western blot, and PCR. We blocked the downstream PKC/MEK pathway of TRPM2 to investigate the mechanism of TRPM2 in pancreatic cancer by CCK8, scratch wound healing, and transwell assays. Overexpressed TRPM2 could promote pancreatic cancer in proliferation, migration, and invasion ability in no matter the cell model or nude mice tumor-bearing model. TRPM2 level is highly negative correlated to the overall survival and progression-free survival time in PA patients, however, it is significantly increased in PA tissue as the tumor stage increases. The transcriptome analysis, GSEA analysis, western-blot, and PCR results indicate TRPM2 is highly correlated with PKC/MAPK pathways. The experiments of PKC/MEK inhibitors added to TRPM2 overexpressed BxPC-3 cell showed that significant inhibition of PA cells happened in CCK8, transwell, and wound-healing assay. TRPM2 may directly activate PKCα by calcium or indirectly activate PKCε and PKCδ by increased DAG in PA, which promote PA by downstream MAPK/MEK pathway activation.

Indexed as

AnimalsCell Line, TumorCell ProliferationHeterograftsHumansMaleMAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase KinasesPancreatic NeoplasmsProtein Kinase CTransfectionTRPM Cation ChannelsMitogen-Activated Protein Kinase KinasesProtein Kinase CTRPM2 protein, humanTRPM Cation Channels

Identifiers

PMID34099637
PMCPMC8184946
OpenAlexW3167867702

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.