Evidence map›Paper›PMID 31670863›Full record

ArticleMolecular oncology2020

Loss of RDM1 enhances hepatocellular carcinoma progression via p53 and Ras/Raf/ERK pathways.

Shi-Lu Chen, Li-Li Liu, Chun-Hua Wang, Shi-Xun Lu, Xia Yang, Yang-Fan He, Chris Zhiyi Zhang, Jing-Ping Yun

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Article
  3. METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025
    Review
  4. RNA mCell investigation · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Landscape of mFrontiers in pharmacology · 2024
    Review
  12. New insights into the regulation of METTL3 and its role in tumors.Cell communication and signaling : CCS · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

8 authors at 2 institutions in 1 country.

Shi-Lu ChenState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.ORCID 0000-0002-0783-0766
Li-Li LiuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Chun-Hua WangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Shi-Xun LuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Xia YangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yang-Fan HeState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Chris Zhiyi ZhangKey Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, China.
Jing-Ping YunState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Sun Yat-sen University · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), with its ineffective therapeutic options and poor prognosis, represents a global threat. In the present study, we show that RAD52 motif 1 (RDM1), a key regulator of DNA double-strand break repair and recombination, is downregulated in HCC tissues and suppresses tumor growth. In clinical HCC samples, low expression of RDM1 correlates with larger tumor size, poor tumor differentiation, and unfavorable survival. In vitro and in vivo data demonstrate that knockdown of RDM1 increases HCC cell proliferation, colony formation, and cell population at G2/M phase, whereas RDM1 overexpression results in the opposite phenotypes. Mechanistically, RDM1 binds to the tumor suppressor p53 and enhances its protein stability. In the presence of p53, RDM1 suppresses the phosphorylation of Raf and ERK. Overexpression of p53 or treatment with ERK inhibitor significantly abolishes cell proliferation induced by the depletion of RDM1. In addition, overexpression of methyltransferase-like 3 markedly induces N6-methyladenosine modification of RDM1 mRNA and represses its expression. Taken together, our study indicates that RDM1 functions as a tumor suppressor and may be a potential prognostic and therapeutic factor for HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsDown-RegulationExtracellular Signal-Regulated MAP KinasesFemaleG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLiver NeoplasmsMAP Kinase Signaling SystemMethylationDNA-Binding ProteinsExtracellular Signal-Regulated MAP KinasesMethyltransferasesMETTL3 protein, humanraf Kinasesras ProteinsRDM1 protein, humanTP53 protein, humanTumor Suppressor Protein p53hepatocellular carcinomaMETTL3p53RDM1RNA methylation

Identifiers

PMID31670863
PMCPMC6998392
OpenAlexW2982536002

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.