Evidence map›Paper›PMID 38229475›Full record

ArticleJournal of cellular and molecular medicine2024

USP11 promotes glycolysis by regulating HIF-1α stability in hepatocellular carcinoma.

Lijun Qiao, Weibin Hu, Linzhi Li, Xin Chen, Liping Liu, Jingbo Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.3field-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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Ubiquitination in cancer: mechanisms and therapeutic opportunities.Cancer communications (London, England) · 2025
    Review
  9. Article
  10. Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. 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 4 institutions in 1 country.

Lijun QiaoCollege of Pharmacy, Shenzhen Technology University, Shenzhen, Guangdong, China.
Weibin HuInstitute for Brain Research and Rehabilitation, South China Normal University, Guangzhou, Guangdong, China.
Linzhi LiLaboratory of Molecular Immunology, State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Xin ChenCollege of Pharmacy, Shenzhen Technology University, Shenzhen, Guangdong, China.
Liping LiuDepartment of Hepatobiliary and Pancreas Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, Guangdong, China.
Jingbo WangCollege of Pharmacy, Shenzhen Technology University, Shenzhen, Guangdong, China.ORCID 0000-0001-5848-9492
Jinan University · CNShenzhen Technology University · CNFudan University · CNSouth China Normal University · CN

Funding

National Natural Science Foundation of China 81903013Youth Innovative Talents Project of Guangdong Education Department 2021KQNCX082
6 · The paper itself

Abstract

Understanding the mechanisms underlying metastasis in hepatocellular carcinoma (HCC) is crucial for developing new therapies against this fatal disease. Deubiquitinase ubiquitin-specific protease 11 (USP11) belongs to the deubiquitinating family and has previously been reported to play a critical role in cancer pathogenesis. Although it has been established that USP11 can facilitate the metastasis and proliferation ability of HCC, the underlying regulatory mechanisms are poorly understood. The primary objective of this research was to reveal hitherto undocumented functions of USP11 during HCC progression, especially those related to metabolism. Under hypoxic conditions, USP11 was found to significantly impact the glycolysis of HCC cells, as demonstrated through various techniques, including RNA-Seq, migration and colony formation assays, EdU and co-immunoprecipitation. Interestingly, we found that USP11 interacted with the HIF-1α complex and maintained HIF-1α protein stability by removing ubiquitin. Moreover, USP11/HIF-1α could promote glycolysis through the PDK1 and LDHA pathways. In general, our results demonstrate that USP11 promotes HCC proliferation and metastasis through HIF-1α/LDHA-induced glycolysis, providing new insights and the experimental basis for developing new treatments for this patient population.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell LineCell Line, TumorGlycolysisHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitThiolester HydrolasesHypoxia-Inducible Factor 1, alpha SubunitThiolester HydrolasesUSP11 protein, humandeubiquitinase ubiquitin-specific protease 11glycolysishepatocellular carcinomahypoxia-inducible transcription factor-1αtumor progression

Identifiers

PMID38229475
PMCPMC10826445
OpenAlexW4390952234

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.