Evidence map›Paper›PMID 40806270›Full record

ArticleInternational journal of molecular sciences2025

Chemosensitizer Effects of Cisplatin- and 5-Fluorouracil-Treated Hepatocellular Carcinomas by Lidocaine.

Teng-Wei Chen, Hsiu-Lung Fan, Shu-Ting Liu, Shih-Ming Huang

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Lidocaine enhances antitumor effects of sorafenib and GW5074 in colorectal cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  2. Article
  3. 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.

Teng-Wei ChenDivision of General Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei City 114, Taiwan.
Hsiu-Lung FanDivision of General Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei City 114, Taiwan.
Shu-Ting LiuDepartment of Biochemistry, National Defense Medical Center, Taipei City 114, Taiwan.
Shih-Ming HuangDepartment of Biochemistry, National Defense Medical Center, Taipei City 114, Taiwan.ORCID 0000-0001-9305-921X

Funding

Teh-Tzer Study Group for Human Medical Research Foundation, Taiwan A1111035 to S-M HuangTri-Service General Hospital, Taiwan TSGH-E-114207 to T-W Chen
6 · The paper itself

Abstract

Approximately 90% of liver cancer cases are classified as hepatocellular carcinomas (HCCs), with chemotherapy and immunotherapy being the most recommended treatment options. While conventional chemotherapy specifically targets rapidly dividing cancer cells, it can also impact on healthy cells that are proliferating quickly. This collateral damage to healthy cells, along with the potential for cancer cells to develop resistance, presents significant challenges for conventional chemotherapy in liver cancer patients. Hepatic artery infusion of chemotherapy (HAIC) generally leads to reduced toxicity and fewer side effects. The process of catheter insertion is usually performed under local anesthesia, with lidocaine being the preferred choice to combine with various chemotherapeutics in HCC treatment. In our study, we explored the effects of repurposing lidocaine in combination with cisplatin or 5-fluorouracil (5-FU) on two HCC cell lines, HepG2 and Hep3B. Our cytotoxicity analysis revealed that lidocaine functions as a chemosensitizer for cisplatin and 5-FU in both HepG2 and Hep3B cells. Specifically, we observed an increase in the subG1 population and a reduction in cytosolic reactive oxygen species in cisplatin- or 5-FU-treated HepG2 and Hep3B cells. Interestingly, lidocaine selectively decreased the reduced/oxidized glutathione ratio in cisplatin- or 5-FU-treated HepG2 cells but not in Hep3B cells. Furthermore, lidocaine induced endoplasmic reticulum stress, apoptosis, mitochondrial membrane depolarization, lipid peroxidation, and autophagy while suppressing cellular proliferation HepG2 and Hep3B cells. In conclusion, our study demonstrates the synergistic potential of combining lidocaine with cisplatin or 5-FU for the treatment of HCC, indicating that lidocaine may serve as an effective chemosensitizer. These findings highlight a new clinical advantage of using repurposing lidocaine as a chemosensitizer in the current HAIC procedure, suggesting that this combination warrants further exploration through rigorous clinical trials. In the future, we can better optimize therapeutic regimens, potentially leading to improved patient outcomes in HCCs.

Indexed as

Antineoplastic AgentsCarcinoma, HepatocellularCisplatinFluorouracilLidocaineLiver NeoplasmsApoptosisCell Line, TumorCell ProliferationDrug SynergismHep G2 CellsHumansReactive Oxygen SpeciesAntineoplastic AgentsCisplatinFluorouracilLidocaineReactive Oxygen Specieschemotherapyendoplasmic reticulum stresshepatic artery infusion chemotherapylidocainereactive oxygen species

Identifiers

PMID40806270
PMCPMC12345720

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LicenceCC BY
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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.