Evidence map›Paper›PMID 41845287›Full record

ArticleBMC cancer2026

CS2164 combined with radiation suppressed tumor growth via γ-H2AX persistence and ROS accumulation.

Shun-Li Peng, Yu-Ling Zhou, Xuexia Liang, Ren-Wei Jiang, Shuai Yang, Qiao-Dan Liu, Xiao-Mou Peng

Abstract read
In one paragraph

Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Shun-Li Peng *Cancer Center, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, China.
Yu-Ling Zhou *Cancer Center, the Central Hospital of Yueyang, Yueyang, Hunan, 414000, China.
Xuexia Liang *Cancer Center, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, China.
Ren-Wei JiangCancer Center, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, China.
Shuai YangCancer Center, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, China.
Qiao-Dan LiuCancer Center, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, China. lqiaodan@mail.sysu.edu.cn.
Xiao-Mou PengCenter of Infectious Diseases, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, 519000, China. pengxmou@mail.sysu.edu.cn.

Funding

the Guangdong Basic and Applied Basic Research Foundation No.2020A1515110599the Health Commission of Guangdong Province No. 20201124205311824the National Natural Science Foundation of China Grant 82303868
6 · The paper itself

Abstract

backgroundCS2164 is an oral multi-target inhibitor that targets angiogenesis-related kinases, mitosis-related kinases, and chronic inflammation-related kinases. However, the added clinical benefit of CS2164 combined with radiation remains unknown.

methodsThe anti-tumor effect of CS2164 combined with radiation were evaluated by CCK-8, colony formation assays and xenograft radiation models (n = 5/per group), based on the hepatocellular carcinoma cells (Huh-7) and cervical cancer cells (HeLa). Meanwhile, the γ-H2AX expression, cell cycle distribution, reactive oxygen species (ROS) assay and transcriptome sequencing analysis of xenografts were performed selected to clarify the mechanism.

resultsCS2164 combined with radiation effectively decreased growth of the above tumor cells, compared with CS2164 or radiation alone. The sensitivity enhancement ratio (SER, SER=D0(control group) / D0(treated group)) of CS2164 was 1.406 in HeLa cells and 1.123 in Huh-7 cells, respectively. Similar antitumor effects were observed in xenograft radiation models. The results of GO, KEGG pathway and PPI analysis screened out a series of genes that related to DNA damage repair process, oxidation-reduction reaction, and multiple cell death types. Therefore, γ-H2AX expression, cell cycle distribution and ROS assay were detected. There was no significant difference in the number of γ-H2AX foci between control and CS2164-treated cells. While the numbers of γ-H2AX foci increased in the CS2164-treated (3µM) cells after radiation (4 Gy) at 3 and 6 h, compared to cells treated with radiation alone (p < 0.05). Meanwhile, more cells were observed to be blocked in G2/M phase after treatment of CS2164 combined with radiation, compared with CS2164 or radiation alone. Moreover, the ROS level increased after treatment of CS2164 combined with radiation, which could be partially rescued by oxidation scavenger, NAC.

conclusionOur study demonstrates anti-tumor efficacy of CS2164 combined with radiation in treatment of malignant tumors.

Indexed as

HistonesLiver NeoplasmsReactive Oxygen SpeciesAnimalsApoptosisCell CycleCell Line, TumorCell ProliferationDNA DamageFemaleHeLa CellsHumansMiceMice, NudeXenograft Model Antitumor AssaysH2AX protein, humanHistonesReactive Oxygen SpeciesCS2164DNA damage responseRadiationRedox imbalance

Identifiers

PMID41845287
PMCPMC13112730

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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.