Evidence map›Paper›PMID 29844385›Full record

ArticleCell death & disease2018

CD24 regulates sorafenib resistance via activating autophagy in hepatocellular carcinoma.

Shuai Lu, Yao Yao, Guolong Xu, Chao Zhou, Yuan Zhang, Jie Sun, Runqiu Jiang, Qing Shao, Yun Chen

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Review
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  6. CD24 as a Novel Radiopharmaceutical Target for Hepatocellular Carcinoma.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
    Article
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  8. Review
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  10. Hepatocellular carcinoma drug resistance models.Cancer cell international · 2025
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  13. Review
  14. Review
  15. Article
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22 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Shuai LuDepartment of Immunology, Nanjing Medical University, Nanjing, 211166, China.
Yao YaoDepartment of Immunology, Nanjing Medical University, Nanjing, 211166, China.
Guolong XuDepartment of Immunology, Nanjing Medical University, Nanjing, 211166, China.
Chao ZhouDepartment of Immunology, Nanjing Medical University, Nanjing, 211166, China.
Yuan ZhangDepartment of Head and Neck Surgery, Cancer biotherapy Center, Jiangsu Cancer Hospital, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210018, China.
Jie SunDepartment of Ophthalmology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Runqiu JiangLiver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. jiangrq@njmu.edu.cn.
Qing ShaoDepartment of Ophthalmology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. 13913862499@139.com.
Yun ChenDepartment of Immunology, Nanjing Medical University, Nanjing, 211166, China. chenyun@njmu.edu.cn.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma is one of most common solid cancers worldwide. Sorafenib is indicated as a treatment for advanced hepatocellular carcinoma (HCC). However, the clinical efficacy of sorafenib has been severely compromised by the development of drug resistance, and the precise mechanisms of drug resistance remain largely unknown. Here we found that a cell surface molecule, CD24, is overexpressed in tumor tissues and sorafenib-resistant hepatocellular carcinoma cell lines. Moreover, there is a positive correlation between CD24 expression levels and sorafenib resistance. In sorafenib-resistant HCC cell lines, depletion of CD24 caused a notable increase of sorafenib sensitivity. In addition, we found that CD24-related sorafenib resistance was accompanied by the activation of autophagy and can be blocked by the inhibition of autophagy using either pharmacological inhibitors or essential autophagy gene knockdown. In further research, we found that CD24 overexpression also leads to an increase in PP2A protein production and induces the deactivation of the mTOR/AKT pathway, which enhances the level of autophagy. These results demonstrate that CD24 regulates sorafenib resistance via activating autophagy in HCC. This is the first report to describe the relationships among CD24, autophagy, and sorafenib resistance. In conclusion, the combination of autophagy modulation and CD24 targeted therapy is a promising therapeutic strategy in the treatment of HCC.

Indexed as

AutophagyDrug Resistance, NeoplasmAnimalsCarcinoma, HepatocellularCD24 AntigenCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMice, NudePrognosisProtein Phosphatase 2Proto-Oncogene Proteins c-aktRNA, MessengerSignal TransductionCD24 AntigenMTOR protein, humanProtein Phosphatase 2Proto-Oncogene Proteins c-aktRNA, MessengerSorafenibTOR Serine-Threonine Kinases

Identifiers

PMID29844385
PMCPMC5974417
OpenAlexW2805076614

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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.