KDM4B在结直肠癌中调控抗肿瘤免疫的机制研究

doi:10.3969/j.issn.1674-8115.2026.08.006

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (8): 1053-1066.doi: 10.3969/j.issn.1674-8115.2026.08.006

• 论著 · 基础研究 • 上一篇

KDM4B在结直肠癌中调控抗肿瘤免疫的机制研究

吴康卉¹, 吴烁², 罗成³, 张元元³(), 李光明¹()

^1.上海交通大学医学院附属新华医院消化内科，上海 200092
^2.中国科学院大学杭州高等研究院药物科学与技术学院，杭州 310024
^3.中国科学院上海药物研究所原创新药研究全国重点实验室，上海 201203

收稿日期:2026-03-24 接受日期:2026-05-11 出版日期:2026-08-06 发布日期:2026-08-06
通讯作者: 李光明，主任医师，博士；电子信箱：liguangming@xinhuamed.com.cn
张元元，研究员，博士；电子信箱：zhangyy@simm.ac.cn。
作者简介:第一联系人：李光明和张元元负责课题的设计与指导，吴康卉与吴烁完成了实验操作、数据分析和文章撰写，罗成和张元元负责实验指导和论文修改。所有作者均阅读并同意了最终稿件的提交。
为共同第一作者（co-first authors）。
基金资助:
国家自然科学基金(82170617)

Mechanistic study of KDM4B in regulating anti-tumor immunity in colorectal cancer

Wu Kanghui¹, Wu Shuo², Luo Cheng³, Zhang Yuanyuan³(), Li Guangming¹()

^1.Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
^2.School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China
^3.State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China

Received:2026-03-24 Accepted:2026-05-11 Online:2026-08-06 Published:2026-08-06
Contact: Li Guangming, E-mail: liguangming@xinhuamed.com.cn
Zhang Yuanyuan, E-mail: zhangyy@simm.ac.cn.
About author:First author contact:Li Guangming and Zhang Yuanyuan were responsible for the project design and supervision. Wu Kanghui and Wu Shuo performed the experiments, conducted the data analysis, and wrote the manuscript. Luo Cheng and Zhang Yuanyuan were responsible for experimental guidance and manuscript revision. All authors have read the last version of paper and consented to its submission.
Supported by:
National Natural Science Foundation of China(82170617)

摘要/Abstract

摘要：

目的·探讨组蛋白赖氨酸去甲基化酶4B（lysine demethylase 4B，KDM4B）在结直肠癌（colorectal cancer，CRC）抗肿瘤免疫中的作用及其分子机制。方法·采用免疫组织化学染色（immunohistochemistry，IHC）检测CRC组织芯片中肿瘤组织和癌旁组织的KDM4B表达水平。利用基因表达综合数据库（Gene Expression Omnibus，GEO）的转录组测序数据集，分析KDM4B mRNA表达量与CRC患者预后、肿瘤内CD8⁺ T细胞浸润程度的相关性，并对KDM4B高表达组和低表达组的CRC样本进行基因集富集分析（Gene Set Enrichment Analysis，GSEA），以探索KDM4B相关的生物学过程。在CRC细胞中敲低KDM4B或使用KDM4B抑制剂B3处理，通过实时荧光定量PCR（quantitative real-time PCR，qPCR）、免疫荧光染色（immunofluorescence，IF）和蛋白质印迹法（Western blotting）检测该处理后细胞中KDM4B相关生物学过程。采用小鼠皮下成瘤实验评估敲低Kdm4b或B3处理在体内对CT26肿瘤增殖能力、肿瘤内CD8⁺ T细胞浸润水平和细胞毒性的影响，并且比较B3治疗、程序性死亡受体-1（programmed cell death protein-1，PD-1）抗体治疗及B3+PD-1抗体联合治疗对小鼠CT26皮下瘤的抗肿瘤作用。结果·IHC结果显示，CRC组织中的KDM4B表达明显高于癌旁组织（P<0.001）。GEO数据集分析的结果显示，KDM4B低表达组的CRC患者表现为更长的生存期以及更高的瘤内CD8⁺ T细胞浸润度（均P<0.05）。GSEA结果显示，KDM4B低表达与Ⅰ型干扰素反应、Th1型细胞毒性反应显著相关。qPCR、IF和蛋白质印迹法的结果显示，敲低KDM4B或B3处理在CRC细胞中能够促进DNA双链断裂、环鸟苷酸-腺苷酸合酶-干扰素基因刺激因子（cyclic GMP-AMP synthase-stimulator of interferon genes，cGAS-STING）信号通路激活、Ⅰ型干扰素和Th1型趋化因子表达增多（均P<0.05）。体内实验显示，敲低Kdm4b或B3处理能够限制CT26肿瘤的生长、促进瘤内CD8⁺ T细胞的浸润和颗粒酶B的表达（均P<0.05）；相较于B3或PD-1抗体单药治疗，B3+PD-1抗体联合治疗对小鼠CT26皮下瘤的抗肿瘤作用更强（均P<0.05）。结论·敲低KDM4B或B3处理可增强CRC细胞的Ⅰ型干扰素和Th1型趋化因子表达，并在体内实验中促进CD8⁺ T细胞抗肿瘤免疫以提高CRC对PD-1抗体的敏感性。

关键词: 结直肠癌, 组蛋白赖氨酸去甲基化酶4B, Ⅰ型干扰素, 肿瘤免疫微环境, 免疫治疗

Abstract:

Objective ·To investigate the role and molecular mechanism of lysine demethylase 4B (KDM4B) in anti-tumor immunity of colorectal cancer (CRC). Methods ·KDM4B expression levels in tumor and para-tumor tissues from a CRC tissue microarray were assessed by immunohistochemistry (IHC) staining. Transcriptomic sequencing datasets from the Gene Expression Omnibus (GEO) database were utilized to analyze the correlations of KDM4B mRNA expression with patient prognosis and intratumoral CD8⁺ T cell infiltration in CRC. Gene Set Enrichment Analysis (GSEA) was conducted on CRC samples with high and low KDM4B expression to identify KDM4B-related biological processes. KDM4B-related biological processes were examined in CRC cells subjected to KDM4B knockdown or B3 treatment using quantitative real-time PCR (qPCR), immunofluorescence (IF) staining, and Western blotting. Mouse subcutaneous tumor models were employed to evaluate the impact of Kdm4b knockdown or B3 treatment on CT26 tumor growth, as well as intratumoral CD8⁺ T cell infiltration and cytotoxicity in vivo. Additionally, the anti-tumor efficacy of B3 treatment, anti-programmed cell death protein-1 (PD-1) antibody therapy, and their combination (B3+anti-PD-1) was compared in CT26 subcutaneous tumor models. Results ·IHC staining results revealed that KDM4B expression was significantly higher in CRC tissues than in para-tumor tissues (P<0.001). Analysis of transcriptomic datasets from the GEO database showed that CRC patients in the KDM4B-low expression group exhibited longer overall survival and increased intratumoral CD8⁺ T cell infiltration (both P<0.05). GSEA results indicated that low KDM4B expression was significantly correlated with typeⅠ interferon response and Th1-type cytotoxic response. qPCR, IF staining, and Western blotting results showed that KDM4B knockdown or B3 treatment promoted DNA double-strand breaks, activated the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway, and increased the expression of type Ⅰ interferons and Th1-type chemokines in CRC cells (all P<0.05). In vivo experiments demonstrated that Kdm4b knockdown or B3 treatment suppressed CT26 tumor growth, and enhanced intratumoral CD8⁺ T cells infiltration and granzyme B expression (all P<0.05). Moreover, compared with B3 or anti-PD-1 antibody monotherapy, the combination of B3 and anti-PD-1 antibody exhibited stronger anti-tumor effects against mouse CT26 subcutaneous tumors (all P<0.05). Conclusion ·KDM4B knockdown or B3 treatment enhances the expression of type Ⅰinterferons and Th1-type chemokines in CRC cells, promotes CD8⁺ T cell-mediated anti-tumor immunity in vivo, and sensitizes CRC to anti-PD-1 antibody therapy.

Key words: colorectal cancer (CRC), lysine demethylase 4B (KDM4B), type Ⅰ interferon, tumor immune microenvironment, immunotherapy

中图分类号:

R735.3

吴康卉, 吴烁, 罗成, 张元元, 李光明. KDM4B在结直肠癌中调控抗肿瘤免疫的机制研究[J]. 上海交通大学学报（医学版）, 2026, 46(8): 1053-1066.

Wu Kanghui, Wu Shuo, Luo Cheng, Zhang Yuanyuan, Li Guangming. Mechanistic study of KDM4B in regulating anti-tumor immunity in colorectal cancer[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026,(8): 1053-1066.

图/表 9

表1 shRNA目的序列

Tab 1 Target sequences of shRNA

shRNA	Target sequence (5'→3')
shControl	TTCTCCGAACGTGTCACGT
shKdm4b#1	GCCAGATCGTCATCACCAAGA
shKdm4b#2	GCTGTAAGATCATGACTTTCC
shKDM4B#1	GCGGCAGACGTATGATGACAT
shKDM4B#2	GCCGGAAGGACATGGTCAAGA

表 2 鼠源基因的qPCR引物序列

Tab 2 Primer sequences for qPCR of mouse genes

Gene	Forward primer (5'→3')	Reverse primer (5'→3')
Ifn-α	TGCCCAGCAGATCAAGAAGG	TCAGGGGAAATTCCTGCACC
Ifn-β	AGCTCCAAGAAAGGACGAACA	GCCCTGTAGGTGAGGTTGAT
Cxcl9	TGGAGTTCGAGGAACCCTAGT	AGGCAGGTTTGATCTCCGTT
Cxcl10	CCAAGTGCTGCCGTCATTTTC	GGCTCGCAGGGATGATTTCAA
Cxcl11	CCACGCTACCTTCTGTGGTT	ATGTTCGTGTGCCTCGTGAT
Actb	GCAAGTGCTTCTAGGCGGAC	AAGAAAGGGTGTAAAACGCAGC

表 3 人源基因的qPCR引物序列

Tab 3 Primer sequences for qPCR of human genes

Gene	Forward primer (5'→3')	Reverse primer (5'→3')
IFN-α	TCGTATGCCAGCTCACCTTT	CAGTCAGCATGGTCCTCTGT
IFN-β	GGCACAACAGGTAGTAGGCG	GTGGAGAAGCACAACAGGAGA
CXCL9	GTGGTGTTCTTTTCCTCTTGGG	ACAGCGACCCTTTCTCACTAC
CXCL10	GCTTCCAAGGATGGACCACA	GCAGGGTCAGAACATCCACT
CXCL11	CTGCCCAAAGGAGTCCAACA	TGTCTCCACCGTAACCACAG
β-actin	GAGAAAATCTGGCACCACACC	ATACCCCTCGTAGATGGGCAC

图1 KDM4B在CRC组织中的表达及其与患者预后、CD8+ T细胞浸润的关系Note： A. KDM4B expression in CRC tissues and para-tumor tissues detected by IHC staining (left: ×5; right: ×20). B. Expression of KDM4B mRNA in CRC and normal specimens from the GSE83889 dataset. C. Overall survival curves of CRC patients stratified by high versus low KDM4B expression in the GSE17536 dataset. D. GSVA scores of activated CD8+ T cells between KDM4B-high and KDM4B-low expression specimens in the GSE83889 dataset. E. The ten most significantly upregulated Hallmark gene sets in CRC samples with low KDM4B expression compared with those with high KDM4B expression identified by GSEA. F. Enrichment analysis of IFN-β targets and Th1 cytotoxic module genes sets in the KDM4B-low expression group versus the KDM4B-high expression group by GSEA. KRAS—kirsten rat sarcoma viral oncogene homolog; IL2—interleukin-2; STAT5—signal transducer and activator of transcription 5; TNF-α—tumour necrosis factor-α; mTORC1—mechanistic target of rapamycin complex 1; MYC—myelocytomatosis oncogene gene; NF-κB—nuclear factor kappa-B; NES—normalized enrichment score.

Fig 1 Expression of KDM4B in CRC tissue and its correlations with patient prognosis and CD8+ T cell infiltration

图2 抑制KDM4B对Ⅰ型干扰素和趋化因子表达水平的影响Note： A. Detection of the efficacy of KDM4B knockdown in CT26 and SW480 cells by Western blotting. B. Detection of H3K9me3 and H3K36me3 expression in CT26 or SW480 cells after KDM4B knockdown by Western blotting. C. Relative mRNA expression levels of the interferons IFN-α/IFN-β and chemokines CXCL9/10/11 in CT26 or SW480 cells following KDM4B knockdown by qPCR. D. Detection of H3K9me3 and H3K36me3 expression in CT26 or SW480 cells afterB3 treatment by Western blotting. E. Cell viability of CT26 or SW480 cells treated with different concentrations of B3.F. Relative mRNA expression levels of the interferons IFN-α/IFN-β and chemokines CXCL9/10/11 in CT26 or SW480 cells followingB3 treatment by qPCR. ①P<0.001, ②P=0.001, compared with the shControl group; ③P<0.001, ④P=0.003, ⑤P=0.006, compared with the Control group.

Fig 2 Effects of KDM4B inhibition on the expression levels of type Ⅰinterferons and Th1 type chemokines

图3 敲低 KDM4B 或B3处理对DNA损伤和cGAS-STING信号轴的影响Note： A. IF staining of γH2A.X (green) in CT26 cells subjected to Kdm4b knockdown or B3 treatment (×63). B. Fluorescence staining of dsDNA (green) and mitochondria (red) in CT26 cells subjected to Kdm4b knockdown or B3 treatment (×63). C. Detection of γH2A.X protein expression in CT26 or SW480 cells after KDM4B knockdown or B3 treatment by Western blotting. D. Detection of the protein expression levels of cGAS-STING axis components in CT26 or SW480 cells following KDM4B knockdown or B3 treatment by Western blotting. F. Relative mRNA expression levels of IFN-α/IFN-β and chemokines CXCL9/10/11 in KDM4B-knockdown CT26 or SW480 cells treated with RU.521. ①P<0.001, ⑤P=0.001, ⑦P=0.004, compared with the shControl group; ②P<0.001, ③P=0.002, compared with the shKdm4b#2 group; ④P<0.001, ⑥P=0.002, ⑧P=0.006, compared with the shKDM4B#2 group.

Fig 3 Effects of KDM4B knockdown or B3 treatment on DNA damage and the cGAS-STING signaling axis

图4 敲低 Kdm4b 或B3处理后CT26细胞体内成瘤和增殖能力的变化Note： A/B. CT26 tumors derived from BALB/c and BALB/c nude mice following Kdm4b knockdown (A) or B3 treatment (B). C/D. Tumor volume and weight of BALB/c and BALB/c nude mice following Kdm4b knockdown (C) or B3 treatment (D). E/F. Body weight of BALB/c mice (E) or BALB/c nude mice (F) implanted with CT26 cells after intratumoral injection of vehicle or B3. G/H. IF staining of Ki-67 in CT26 tumor tissues after Kdm4b knockdown (G) or B3 treatment (H) in BALB/c mice (×20). ①P<0.001, ④P=0.002, compared with the shControl group; ②P<0.001, ③P=0.003, ⑤P=0.033, ⑥P=0.017, compared with the Control group.

Fig 4 Tumorigenic and proliferative capacities of CT26 cells in vivo following Kdm4b knockdown or B3 treatment

图5 体内研究中敲低 Kdm4b 或B3处理对DNA损伤、CD8+ T细胞浸润和GZMB表达的影响Note： A/B. Detection of γH2A.X expression in tumor tissues from BALB/c mice with Kdm4b knockdown (A) or B3 treatment (B) by IF staining (×20). C/D. Relative mRNA expression levels of type Ⅰ interferons Ifn-α/Ifn-β and Th1 type chemokines Cxcl9/10/11 in tumor tissues from BALB/c mice with Kdm4b knockdown (C) or B3 treatment (D) detected by qPCR. E/F. Detection of CD8⁺ T cells infiltration in CT26 tumor tissues after Kdm4b knockdown (E) or B3 treatment (F) in BALB/c mice by IF staining (×20). G/H. Detection of GZMB expression in CT26 tumor tissues after Kdm4b knockdown (G) or B3 treatment (H) in BALB/c mice by IF staining (×20). ①P<0.001, ③P=0.006, compared with the shControl group; ②P<0.001, ④P=0.001, compared with the Control group.

Fig 5 Effects of Kdm4b knockdown or B3 treatment on DNA damage, CD8⁺ T cells infiltration, and GZMB expression in vivo

图6 体内研究中B3联合PD-1抗体治疗对CT26肿瘤生长、肿瘤内CD8+ T细胞浸润和GZMB表达的影响Note： A. CT26 tumors derived from BALB/c mice among the four groups (Control, anti-PD-1, B3, and B3+anti-PD-1). B/C. Tumor volume (B) and weight (C) of BALB/c mice subcutaneously implanted with CT26 cells in each group. D.Body weight of BALB/c mice subcutaneously implanted with CT26 cells in each group. E/F. IF staining of CD8⁺ T cells (E) and GZMB+ cells (F) in CT26 tumor tissues among the four groups (×20). ①P<0.001, ②P=0.004, ④P=0.006, ⑥P=0.001, ⑦P=0.047, ⑧P=0.002, ⑨P=0.046, compared with the Control group; ③P=0.004, ⑤P=0.023, B3 group vs B3+anti-PD-1 group.

Fig 6 Effects of B3 combined with anti-PD-1 antibody therapy on CT26 tumor growth, intratumoral CD8⁺ T cells infiltration, and GZMB expression in vivo

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KDM4B在结直肠癌中调控抗肿瘤免疫的机制研究

Mechanistic study of KDM4B in regulating anti-tumor immunity in colorectal cancer

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