Evidence map›Paper›PMID 36529521›Full record

ArticleCancer science2023

A feedback loop between NONHSAT024276 and PTBP1 inhibits tumor progression and glycolysis in HCC by increasing the PKM1/PKM2 ratio.

Yuwei Li, Xia Chen, Hengliu Huang, Ling Liao, Huimin Chong, Guangyao Li, Tao Yuan, Weiping Lu, Shaoli Deng, Qing Huang

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Frontiers in pharmacology · 2024
    Review
  8. 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

10 authors at 1 institution in 1 country.

Yuwei LiDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.ORCID https://orcid.org/0000-0002-6579-2526
Xia ChenDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Hengliu HuangDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Ling LiaoDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Huimin ChongDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Guangyao LiDepartment of Hepatobiliary Surgery, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Tao YuanDepartment of Hepatobiliary Surgery, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Weiping LuDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Shaoli DengDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Qing HuangDepartment of Laboratory Medicine, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Army Medical University · CN

Funding

Clinical Medical Research Talents Funding Project 2019XLC1010National Natural Science Foundation of China 82172370
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies with a hallmark of aberrant metabolism. The mechanism of long noncoding RNAs (lncRNAs) underlying the aggressive behaviors and glycolysis of HCC is poorly understood. In this study, we identified, via microarray, novel lncRNA NONHSAT024276 as a potential tumor suppressor in HCC. The downregulation of NONHSAT024276 closely correlated with larger tumor volume and higher aspartate transaminase levels. Functional experiments were performed to verify the role of NONHSAT024276 in HCC progression, and the negative effects of NONHSAT024276 expression on cell proliferation and migration were identified. Mechanistically, NONHSAT024276 directly bound to polypyrimidine tract-binding protein 1 (PTBP1), downregulating it and forming a feedback loop. Furthermore, NONHSAT024276 increased the ratio of M1 and M2 isoforms of pyruvate kinase (PKM1/PKM2) and also obstructed the PTBP1/PKM-mediated glycolysis. Finally, the rescue assays confirmed that NONHSAT024276 functioned in HCC via downregulating PTBP1 to increase the PKM1/PKM2 ratio. Hence, this study supported a model in which NONHSAT024276 downregulated PTBP1 and formed a feedback loop to increase the PKM1/PKM2 ratio to inhibit glycolysis and progression of HCC, opening new prospects for preventing or treating HCC.

Indexed as

Carcinoma, HepatocellularHeterogeneous-Nuclear RibonucleoproteinsLiver NeoplasmsPolypyrimidine Tract-Binding ProteinRNA, Long NoncodingCell Line, TumorCell ProliferationFeedbackGlycolysisHumansPyruvate KinaseHeterogeneous-Nuclear RibonucleoproteinsPolypyrimidine Tract-Binding ProteinPTBP1 protein, humanPyruvate KinaseRNA, Long Noncodingglycolysishepatocellular carcinomalncRNAPTBP1pyruvate kinase

Identifiers

PMID36529521
PMCPMC10067414
OpenAlexW4311868441

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.