Evidence map›Paper›PMID 38591121›Full record

ArticleActa biochimica et biophysica Sinica2024

Carfilzomib activates ER stress and JNK/p38 MAPK signaling to promote apoptosis in hepatocellular carcinoma cells.

Yao Deng, Yujie Li, Mingyue Yang, Yang Gao, Xuling Luo, Hanbin Chen, Meng Guo, Xuefeng Yang, Yongzhang Liu, Jun He and 2 more

Abstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
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  5. Eupatilin alleviates right ventricular fibrosis in rats with pulmonary hypertension induced by monocrotaline.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  6. Article
  7. Article
  8. Article
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  10. Oncology research · 2025
    Article
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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

12 authors.

Yao DengDepartment of Gastroenterology and Hunan Provincial Clinical Research Center for Metabolic Associated Fatty Liver Disease, The Affiliated Nanhua Hospital and Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Yujie LiSchool of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Mingyue YangSchool of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Yang GaoSchool of Public Health, Fudan University, Shanghai 200032, China.
Xuling LuoDepartment of Gastroenterology and Hunan Provincial Clinical Research Center for Metabolic Associated Fatty Liver Disease, The Affiliated Nanhua Hospital and Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Hanbin ChenDepartment of Oncology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China.
Meng GuoDepartment of Gastroenterology and Hunan Provincial Clinical Research Center for Metabolic Associated Fatty Liver Disease, The Affiliated Nanhua Hospital and Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Xuefeng YangDepartment of Gastroenterology and Hunan Provincial Clinical Research Center for Metabolic Associated Fatty Liver Disease, The Affiliated Nanhua Hospital and Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Yongzhang LiuSchool of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Jun HeDepartment of Gastroenterology and Hunan Provincial Clinical Research Center for Metabolic Associated Fatty Liver Disease, The Affiliated Nanhua Hospital and Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Bin LuDepartment of Gastroenterology and Hunan Provincial Clinical Research Center for Metabolic Associated Fatty Liver Disease, The Affiliated Nanhua Hospital and Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Naxin LiuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most prevalent and deadly cancers in the world, which is frequently diagnosed at a late stage. HCC patients have a poor prognosis due to the lack of an efficacious therapeutic strategy. Approved drug repurposing is a way for accelerating drug discovery and can significantly reduce the cost of drug development. Carfilzomib (CFZ) is a second-generation proteasome inhibitor, which is highly efficacious against multiple myeloma and has been reported to possess potential antitumor activities against multiple cancers. However, the underlying mechanism of CFZ on HCC is still unclear. Here, we show that CFZ inhibits the proliferation of HCC cells through cell cycle arrest at the G2/M phase and suppresses the migration and invasion of HCC cells by inhibiting epithelial-mesenchymal transition. We also find that CFZ promotes reactive oxygen species production to induce endoplasmic reticulum (ER) stress and activate JNK/p38 MAPK signaling in HCC cells, thus inducing cell death in HCC cells. Moreover, CFZ significantly inhibits HCC cell growth in a xenograft mouse model. Collectively, our study elucidates that CFZ impairs mitochondrial function and activates ER stress and JNK/p38 MAPK signaling, thus inhibiting HCC cell and tumor growth. This indicates that CFZ has the potential as a therapeutic drug for HCC.

Indexed as

ApoptosisCarcinoma, HepatocellularEndoplasmic Reticulum StressLiver NeoplasmsOligopeptidesAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansMAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, Nudep38 Mitogen-Activated Protein KinasescarfilzomibOligopeptidesp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciescarfilzomibER stresshepatocellular carcinomaJNK/p38 MAPK signalingproteasome inhibitor

Identifiers

PMID38591121
PMCPMC11177107

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Registered trials

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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.