Evidence map›Paper›PMID 25883212›Full record

ArticleOncotarget2015

LLL12, a novel small inhibitor targeting STAT3 for hepatocellular carcinoma therapy.

Mingxin Zuo, Chenglong Li, Jiayuh Lin, Milind Javle

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Enhancer regulation in cancer: from epigenetics to mArchives of pharmacal research · 2025
    Review
  4. Review
  5. Article
  6. Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024
    Review
  7. The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Phosphotyrosine isosteres: past, present and future.Organic & biomolecular chemistry · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Targeting Transcription Factors for Cancer Treatment.Molecules (Basel, Switzerland) · 2018
    Review
  17. Article
  18. Article
  19. Frontiers in pharmacology · 2018
    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

4 authors at 3 institutions in 1 country.

Mingxin ZuoDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Chenglong LiDivision of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA.
Jiayuh LinCenter for Childhood Cancer, The Research Institute at Nationwide Children's Hospital, Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, OH 43205, USA.
Milind JavleDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
The University of Texas MD Anderson Cancer Center · USNationwide Children's Hospital · USThe Ohio State University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672NCI NIH HHS P30CA016672
6 · The paper itself

Abstract

The constitutive activation of signal transducer and activator of transcription 3 (STAT3) is frequently detected in clinical incidences of hepatocellular carcinoma (HCC) but not in normal human hepatocytes. STAT3 signaling plays pivotal roles in angiogenesis, survival, metastasis, and growth of HCC. Recent evidence suggests that the blockade of aberrant STAT3 pathways can be exploited as a therapeutic strategy for HCC. We have developed the novel small molecular STAT3 inhibitor LLL12 on the basis of curcumin structure using computer-aided rational design. LLL12 has shown antitumor activity in various solid tumors including breast, brain, pancreatic cancer, and glioblastoma in vitro and in vivo. In this study, we hypothesized LLL12 inhibits STAT3 phosphorylation at tyrosine 705 (Y705) in HCC and show antitumor activity in HCC in vitro and in vivo. Our results show that LLL12 selectively inhibited HCC cell proliferation and induced apoptosis in SNU387, SNU398, SNU449, and Hep3B HCC cells in vitro. Furthermore, LLL12 at 5 mg/kg/day significantly inhibited the growth of SNU398 xenografts in nude mice. Collectively, our results indicate that LLL12 could be used to target STAT3 for the effective prevention or treatment of HCC.

Indexed as

AnimalsAnthraquinonesApoptosisBlotting, WesternCarcinoma, HepatocellularCell CycleCell ProliferationFemaleFlow CytometryFluorescent Antibody TechniqueHumansLiver NeoplasmsMiceMice, NudePhosphorylationReal-Time Polymerase Chain ReactionAnthraquinonesLLL12 compoundRNA, MessengerSTAT3 Transcription FactorSulfonamideshepatocellular carcinomaLLL12small molecular inhibitorSTAT3

Identifiers

PMID25883212
PMCPMC4484430
OpenAlexW1804193440

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.