Evidence map›Paper›PMID 40082280›Full record

ArticleJournal of cancer research and clinical oncology2025

A novel strategy for sorafenib-resistant hepatocellular carcinoma: autotaxin Inhibition by PF-8380.

Bong Jun Kwak, Jung Hyun Park, Ok-Hee Kim, Dosang Lee, Tae Ho Hong, Sang Chul Lee, Kee-Hwan Kim, Ho Joong Choi, Say-June Kim

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cancer research and clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

9 authors.

Bong Jun Kwak *Department of Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea.
Jung Hyun Park *Department of Surgery, Eunpyeong St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, 03312, Republic of Korea.
Ok-Hee KimCatholic Central Laboratory of Surgery, Institute of Biomedical Industry, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Dosang LeeCatholic Central Laboratory of Surgery, Institute of Biomedical Industry, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Tae Ho HongCatholic Central Laboratory of Surgery, Institute of Biomedical Industry, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Sang Chul LeeDepartment of Surgery, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon, 34943, Republic of Korea.
Kee-Hwan KimCatholic Central Laboratory of Surgery, Institute of Biomedical Industry, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Ho Joong ChoiDepartment of Surgery, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Say-June KimCatholic Central Laboratory of Surgery, Institute of Biomedical Industry, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea. sayjunekim@catholic.ac.kr.

Funding

Hanmi Science.Co.,Ltd. 5-2020-D0644-00003
6 · The paper itself

Abstract

By inhibiting the conversion of lysophosphatidylcholine into lysophosphatidic acid, a process pivotal to tumor progression, the autotaxin (ATX) inhibitor PF-8380 offers a new anticancer therapeutic strategy, distinct from the action mechanism of sorafenib. This study explored the potential anticancer effects of the PF-8380 on hepatocellular carcinoma (HCC) cells, especially sorafenib-resistant strains. The investigation included both in vitro and in vivo experiments to evaluate the impact of PF-8380 treatment on epithelial-mesenchymal transition (EMT) and autophagy markers. An orthotopic HCC model served as the in vivo platform. PF-8380 showed a significant reduction in cell viability in both sorafenib-susceptible and resistant HCC cells. It effectively altered EMT by increasing E-cadherin and reducing Snail levels, and inhibited autophagy, as indicated by changes in LC3 and p62 markers. These effects were consistently observed in the orthotopic HCC mouse model, reinforcing PF-8380's potential as a dual inhibitor of EMT and autophagy in HCC treatment. Our research indicates that PF-8380 could provide substantial therapeutic benefits in the treatment of HCC, even in cases resistant to sorafenib, primarily by suppressing both EMT and autophagy processes.

Indexed as

Antineoplastic AgentsCarcinoma, HepatocellularDrug Resistance, NeoplasmLiver NeoplasmsNiacinamidePhenylurea CompoundsPhosphoric Diester HydrolasesAnimalsAutophagyCell Line, TumorEpithelial-Mesenchymal TransitionHumansLysophospholipase DMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsLysophospholipase DNiacinamidePhenylurea CompoundsPhosphoric Diester HydrolasesSorafenibAutophagyAutotaxin inhibitorEpithelial-mesenchymal transition (EMT)Hepatocellular carcinomaSorafenib

Identifiers

PMID40082280
PMCPMC11906571

What Socratic 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 Socratic graph.