Evidence map›Paper›PMID 35557985›Full record

ArticleOxidative medicine and cellular longevity2022

LncRNA-MALAT1 Regulates Cancer Glucose Metabolism in Prostate Cancer via MYBL2/mTOR Axis.

Xiangyu Mu, Zhou Shen, Yao Lin, Jun Xiao, Kaiguo Xia, Congyun Xu, Biao Chen, Ronghua Shi, Anyang Zhu, Xinzhe Sun and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. 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
2.4field-weighted citation impact, top 10% 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, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
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

13 authors at 2 institutions in 1 country.

Xiangyu MuDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-5727-5035
Zhou ShenDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-0521-4927
Yao LinDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-6455-928X
Jun XiaoDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0001-9012-1110
Kaiguo XiaDepartment of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.ORCID https://orcid.org/0000-0002-6795-6547
Congyun XuDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0003-4933-4338
Biao ChenDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-9297-9361
Ronghua ShiMOE Key Laboratory for Cellular Dynamics, CAS Key Laboratory of Brain Function and Disease, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230026, China.ORCID https://orcid.org/0000-0002-4413-3169
Anyang ZhuDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0003-1048-171X
Xinzhe SunDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-1285-4172
Tao TaoDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0003-1609-9079
Xiaoyuan SongDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-9011-5033
Qiang XuanDepartment of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science & Technology of China (USTC), Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0001-6208-7656
University of Science and Technology of China · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is known that the long noncoding RNAs (lncRNA) MALAT1 is associated with tumorigenesis and progression in various cancers; however, its functions and mechanisms in prostate cancer (PCa) initiation and progression are still unknown. In the present study, our findings revealed that MALAT1 plays a critical part in regulating PCa proliferation and glucose metabolism. Knockdown of MALAT1 affects the protein and mRNA levels of MYBL2. In addition, MALAT1 enhances the phosphorylation level of mTOR pathway by upregulating MYBL2. Knockdown of MALAT1 or MYBL2 in PCa cell lines significantly inhibits their proliferation capacity. Silencing MALAT1/MYBL2/mTOR axis in PCa cell lines affects their glycolysis and lactate levels, and we verified these findings in mice. Furthermore, we explored the underlying tumorigenesis functions of MYBL2 in PCa and found that high expression of MYBL2 was positively associated with TNM stage, Gleason score, PSA level, and poor survival rate in PCa patients. Taken together, our research suggests that MALAT1 controls cancer glucose metabolism and progression by upregulating MYBL2-mTOR axis.

Indexed as

Cell Cycle ProteinsGlucoseMicroRNAsProstatic NeoplasmsRNA, Long NoncodingTrans-ActivatorsAnimalsCarcinogenesisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMiceTOR Serine-Threonine KinasesCell Cycle ProteinsGlucoseMALAT1 long non-coding RNA, humanMicroRNAsMTOR protein, humanMYBL2 protein, humanRNA, Long NoncodingTOR Serine-Threonine KinasesTrans-Activators

Identifiers

PMID35557985
PMCPMC9086835
OpenAlexW4225306912

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.