Evidence map›Paper›PMID 32395503›Full record

ArticleAnnals of translational medicine2020

Sam68 promotes aerobic glycolysis in colorectal cancer by regulating PKM2 alternative splicing.

Jing Zhao, Jiuming Li, Waseem Hassan, Dongyan Xu, Xue Wang, Zhaohui Huang

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Oncology letters · 2025
    Article
  6. Review
  7. Article
  8. Predictive Value of Normalized Lactate Load for Patients with Acute Type A Aortic Dissection: Based on the MIMIC-IV Database.Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia · 2025
    Article
  9. Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

6 authors at 3 institutions in 2 countries.

Jing ZhaoWuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Wuxi 214062, China.
Jiuming LiWuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Wuxi 214062, China.
Waseem HassanDepartment of Pharmacy, COMSATS University Islamabad, Lahore Campus, Lahore, Pakistan.
Dongyan XuLaboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University, Wuxi 214062, China.
Xue WangLaboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University, Wuxi 214062, China.
Zhaohui HuangWuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Wuxi 214062, China.
Jiangnan University · CNWuxi Fourth People's Hospital · CNCOMSATS University Islamabad · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSam68, an RNA-binding protein, exerts oncogenic functions in several types of cancer. However, the specific functions and mechanisms of Sam68 in colorectal cancer (CRC) had not been previously clarified. Pyruvate kinase muscle (PKM)2 is the key rate-limiting enzyme in glycolysis, and PKM2 maintains the glycolysis-dominant energy metabolism in most cancer cells.

methodsCCK8 assay was performed to show the effect of Sam68 on cell growth. Pyruvate kinase activity and lactate detection assays were performed to analyze the effects of Sam68 on aerobic glycolysis. RNA immunoprecipitation (RIP) was used to detect the binding of Sam68 to the

resultsGain-of-function and loss-of-function studies showed that ectopic expression of Sam68 promoted glycolysis and cell proliferation in CRC cells, whereas Sam68 knockdown inhibited glycolysis and cell proliferation. Mechanically, Sam68 modulated the expression profile of pyruvate kinase (PKM2 or PKM1) by regulating its alternative splicing. Overexpression of Sam68 was associated with decreased

conclusionsThese findings suggested that Sam68 affected cell growth and glycolysis pathway by regulating the alternative splicing and expression of PKM2 in CRC.

Indexed as

alternative splicingColorectal cancer (CRC)glycolysispyruvate kinase muscle 2 (PKM2)sam68

Identifiers

PMID32395503
PMCPMC7210197
OpenAlexW3015842226

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.