Evidence map›Paper›PMID 26082485›Full record

ArticleThe Journal of biological chemistry2015

Steroid Receptor Coactivator 1 Promotes Human Hepatocellular Carcinoma Progression by Enhancing Wnt/β-Catenin Signaling.

Zhangwei Tong, Ming Li, Wei Wang, Pingli Mo, Li Yu, Kun Liu, Wenjing Ren, Wengang Li, Hao Zhang, Jianming Xu and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Targeting RORγ inhibits the growth and metastasis of hepatocellular carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. β-Catenin signaling in hepatocellular carcinoma.The Journal of clinical investigation · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

11 authors at 3 institutions in 2 countries.

Zhangwei TongFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China, the Engineering Research Center of Molecular Diagnostics, Ministry of Education, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Ming LiFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China, the Department of Hepatobiliary Pancreas and Vessel Surgery, Chenggong Hospital of Xiamen University, Xiamen, Fujian 361003, China.
Wei WangFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Pingli MoFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Li YuFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Kun LiuFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China, the Department of Pathology, Chenggong Hospital of Xiamen University, Xiamen, China.
Wenjing RenFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Wengang Lithe Department of Hepatobiliary Pancreas and Vessel Surgery, Chenggong Hospital of Xiamen University, Xiamen, Fujian 361003, China.
Hao Zhangthe Cancer Research Center at Shantou University Medical College, Shantou, Guangdong 515041, China, and.
Jianming Xuthe Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030.
Chundong YuFrom the State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China, the Engineering Research Center of Molecular Diagnostics, Ministry of Education, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China, cdyu@xmu.edu.cn.
Xiamen University · CNBaylor College of Medicine · USShantou University Medical College · CN

Funding

The Role of SRC-1 in Breast CancerR01CA112403 · NCI · BAYLOR COLLEGE OF MEDICINE · PI XU, JIANMING · 2006 to 2016
$2.9M
NCOA6, A Novel Tumor Suppressor of Endometrial CancerR01CA193455 · NCI · BAYLOR COLLEGE OF MEDICINE · PI XU, JIANMING · 2016 to 2021
$1.9M
NCI NIH HHS R01 CA112403NCI NIH HHS R01 CA193455
6 · The paper itself

Abstract

Steroid receptor coactivator 1 (SRC-1) is a transcriptional coactivator not only for steroid receptors, such as androgen receptor and estrogen receptor, but also for other transcription factors. SRC-1 has been shown to play an important role in the progression of breast cancer and prostate cancer. However, its role in liver cancer progression remains unknown. In this study, we report that SRC-1 was overexpressed in 25 (62.5%) of 40 human hepatocellular carcinoma (HCC) specimens. Down-regulation of SRC-1 decreased HCC cell proliferation and impaired tumor maintenance in HCC xenografts. Knockdown of SRC-1 reduced protein levels of the proliferation marker proliferating cell nuclear antigen (PCNA) and the oncogene c-Myc. Knockout of SRC-1 in mice reduced diethylnitrosamine/CCl4-induced tumor formation in the liver and the expression of c-Myc and PCNA in liver tumors. SRC-1 promoted c-Myc expression, at least in part, by directly interacting with β-catenin to enhance Wnt/β-catenin signaling. Consistent with these results, the expression of SRC-1 was positively correlated with PCNA expression in human HCC specimens, and the expression levels of c-Myc in SRC-1-positive HCC specimens were higher than in SRC-1-negative HCC specimens. In addition, SRC-1 and SRC-3 were co-overexpressed in 47.5% of HCC specimens, and they cooperated to promote HCC cell proliferation. Simultaneous down-regulation of SRC-1 and SRC-3 dramatically inhibited HCC cell proliferation. Our results demonstrate that SRC-1 promotes HCC progression by enhancing Wnt/β-catenin signaling and suggest that SRC-1 is a potential therapeutic molecular target for HCC.

Indexed as

Animalsbeta CateninCarcinoma, HepatocellularCell ProliferationGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceNuclear Receptor Coactivator 1Nuclear Receptor Coactivator 3Proliferating Cell Nuclear AntigenProto-Oncogene Proteins c-mycWnt Signaling PathwayXenograft Model Antitumor Assaysbeta CateninMYC protein, humanNCOA3 protein, humanNuclear Receptor Coactivator 1Nuclear Receptor Coactivator 3Proliferating Cell Nuclear AntigenProto-Oncogene Proteins c-myccell proliferationhepatocellular carcinomaMyc (c-Myc)steroid receptor coactivator (SRC-1)transcriptional coactivatorWnt signaling

Identifiers

PMID26082485
PMCPMC4513118
OpenAlexW1549513369

What OpenQuestion 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 OpenQuestion graph.