Evidence mapPaperPMID 32144382Full record

ArticleCell death and differentiation2020

The lipogenic LXR-SREBF1 signaling pathway controls cancer cell DNA repair and apoptosis and is a vulnerable point of malignant tumors for cancer therapy.

Bo Yang, Bin Zhang, Zhifei Cao, Xingdong Xu, Zihe Huo, Pan Zhang, Shufen Xiang, Zhe Zhao, Chunping Lv, Mei Meng and 5 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Chicoric acid enhanced brain cholesterol efflux and reduced Aβ pathology via LXR-ABCA1 signaling in Alzheimer's models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Lipid Metabolism as a Potential Target of Liver Cancer.Journal of hepatocellular carcinoma · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Bo Yang *Department of General Surgery, The Third Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Bin Zhang *Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Zhifei Cao *Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China. hunancao@163.com.
Xingdong XuDepartment of General Surgery, The People's Hospital of China, Three Gorges University, Yichang, 443000, P. R. China.
Zihe HuoCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Pan ZhangCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Shufen XiangCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Zhe ZhaoCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Chunping LvCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Mei MengCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Gaochuan ZhangDepartment of Bioinformatics, College of Basic Medical Science, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Liang DongDepartment of Pathology, College of Basic Medical Science, Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Shucheng ShiDepartment of General Surgery, The Third Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Lan YangDepartment of General Surgery, The Third Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215123, P. R. China.
Quansheng ZhouCyrus Tang Hematology Center, Jiangsu Institute of Hematology, Soochow University, Suzhou, Jiangsu, 215123, P. R. China. zhouqs@suda.edu.cn.
Soochow University · CNChina Three Gorges University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells are defective in DNA repair, so they experience increased DNA strand breaks, genome instability, gene mutagenesis, and tumorigenicity; however, multiple classic DNA repair genes and pathways are strongly activated in malignant tumor cells to compensate for the DNA repair deficiency and gain an apoptosis resistance. The mechanisms underlying this phenomenon in cancer are unclear. We speculate that a key DNA repair gene or signaling pathway in cancer has not yet been recognized. Here, we show that the lipogenic liver X receptor (LXR)-sterol response element binding factor-1 (SREBF1) axis controls the transcription of a key DNA repair gene polynucleotide kinase/phosphatase (PNKP), thereby governing cancer cell DNA repair and apoptosis. Notably, the PNKP levels were significantly reduced in 95% of human pancreatic cancer (PC) patients, particularly deep reduction for sixfold in all of the advanced-stage PC cases. PNKP is also deficient in three other types of cancer that we examined. In addition, the expression of LXRs and SREBF1 was significantly reduced in the tumor tissues from human PC patients compared with the adjacent normal tissues. The newly identified LXR-SREBF1-PNKP signaling pathway is deficient in PC, and the defect in the pathway contributes to the DNA repair deficiency in the cancer. Strikingly, further diminution of the vulnerable LXR-SREBF1-PNKP signaling pathway using a small molecule triptonide, a new LXR antagonist identified in this investigation, at a concentration of 8 nM robustly activated tumor-suppressor p53 and readily elevated cancer cell DNA strand breaks over an apoptotic threshold, and selectively induced PC cell apoptosis, resulting in almost complete elimination of tumors in xenograft mice without obvious complications. Our findings provide new insight into DNA repair and apoptosis in cancer, and offer a new platform for developing novel anticancer therapeutics.

Indexed as

ApoptosisDNA RepairLipogenesisSignal TransductionAnimalsCarcinogenesisCell Line, TumorDNA Breaks, Double-StrandedDNA Repair EnzymesFemaleGene Expression Regulation, NeoplasticHumansLiver X ReceptorsMice, NudeMitosisModels, BiologicalDNA Repair EnzymesLiver X ReceptorsPhosphotransferases (Alcohol Group Acceptor)PNKP protein, humanRNA, MessengerSREBF1 protein, humanSterol Regulatory Element Binding Protein 1triptonideTriterpenesTumor Suppressor Protein p53

Identifiers

PMID32144382
PMCPMC7370224
OpenAlexW3009742610

What Socratic holds

Textmetadata
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 Socratic graph.