Evidence map›Paper›PMID 33616859›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2021

UCHL3 promotes aerobic glycolysis of pancreatic cancer through upregulating LDHA expression.

Y Fan, D Hu, D Li, C Ma, Y Tang, Q Tao, L Deng, D Tang

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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 31 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

8 authors at 1 institution in 1 country.

Y Fan *The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
D Hu *The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
D LiThe Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
C MaThe Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
Y TangThe Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
Q TaoThe Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
L DengThe Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China.
D TangThe Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen City, 518107, Guangdong Province, China. tangdi@sysu.edu.cn.ORCID http://orcid.org/0000-0002-1480-1584
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAerobic glycolysis has a pivotal role in the carcinogenic process. The current understanding of the functional role and mechanism of UCHL3-related aerobic glycolysis in pancreatic cancer is far from comprehensive, therefore requires an in-depth analysis on this aspect.

methodsIn the present research, the expressions of ubiquitin carboxyl-terminal hydrolase L3 (UCHL3), lactate dehydrogenase A (LDHA) and Forkhead box protein M1 (FOXM1) were detected by qRT-PCR, Western blot and immunohistochemistry. The effects of UCHL3 knockdown or overexpression on pancreatic cancer cells were examined by determining cell viability and colony formation. Aerobic glycolysis was assessed according to glucose uptake, lactic acid production, and lactate dehydrogenase (LDH) activity. Dual-luciferase reporter assay was performed to detect LDHA promoter activity.

resultsThe results showed that UCHL3 expression was significantly increased in the pancreatic cancer tissues and cells, and that knocking down UCHL3 noticeably inhibited cell viability and aerobic glycolysis. Further investigations revealed that LDHA expression was promoted by UCHL3 and could be reduced by shFOXM1, and that low-expressed LDHA partly reversed the inhibition of aerobic glycolysis induced by overexpressed UCHL3.

conclusionsTo conclude, this study demonstrates that UCHL3 plays a carcinogenic role by promoting aerobic glycolysis in pancreatic cancer, suggesting that UCHL3 may be a potential diagnostic and therapeutic target for the treatment of cancer.

Indexed as

Up-RegulationAerobiosisCell Line, TumorCell ProliferationForkhead Box Protein M1GlucoseGlycolysisHumansLactate Dehydrogenase 5PancreasPancreatic NeoplasmsUbiquitin ThiolesteraseForkhead Box Protein M1FOXM1 protein, humanGlucoseLactate Dehydrogenase 5Ubiquitin ThiolesteraseUCHL3 protein, humanGlycolyticLactate dehydrogenase APancreatic cancerUbiquitin carboxyl-terminal hydrolase L3

Identifiers

PMID33616859
OpenAlexW3130367283

What OpenQuestion holds

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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.