AbstractChromodomain helicase DNA-binding protein (CHD) gene family, an ATP (adenosine triphosphate) -dependent chromatin remodeler family, is involved in multiple developmental process and tumor development. However, there have been none pan-cancer analyses of this family. The expression levels, survival profiles, mutation profiles and immune infiltration of the CHD family genes from TCGA and TARGET database were analyzed using online tools or R packages.

摘要染色体结构域解旋酶DNA结合蛋白（CHD）基因家族是一个依赖ATP（三磷酸腺苷）的染色质重塑家族，参与多种发育过程和肿瘤的发展。但是，尚未对该家族进行泛癌分析。使用在线工具或R软件包分析了来自TCGA和TARGET数据库的CHD家族基因的表达水平，存活谱，突变谱和免疫浸润。

Interestingly, all types of CHD gene expressions were associated with the prognosis of Neuroblastoma, Acute lymphoblastic leukemia-Phase 3 and Acute Myeloid Leukemia (All P < 0.05). Knock down of CHD7 and CHD9 in K562 (human erythromyeloblastoid leukemia) and HEC-1-B (human endometrial adenocarcinoma) cells significantly inhibit cell proliferation and migration (P < 0.05).

有趣的是，所有类型的CHD基因表达均与神经母细胞瘤，急性淋巴细胞白血病3期和急性髓细胞白血病的预后相关（均P<0.05）。敲除K562（人红髓母细胞白血病）和HEC-1-B（人子宫内膜腺癌）细胞中的CHD7和CHD9可显着抑制细胞增殖和迁移（P<0.05）。

Proliferation, colony formation and migration assays were performed in CHD7 and CHD9 knockdown K562 and HBC-1-B cell lines. Mechanisms were also analyzed by PPI and GO ontology for our experiments. Histone modification, especially the methylation of H3K4, might be involved in CHD7 and CHD9 related oncogenesis.

在CHD7和CHD9敲低的K562和HBC-1-B细胞系中进行增殖，集落形成和迁移测定。。组蛋白修饰，特别是H3K4的甲基化，可能与CHD7和CHD9相关的肿瘤发生有关。

Through bioinformatic analysis, we showed CHD genes significantly affected the prognosis of different tumor types, including childhood tumor. Our findings provide new insights into the function and mechanism of CHD gene family, especially in CHD7 and CHD9..

通过生物信息学分析，我们发现CHD基因显着影响不同肿瘤类型的预后，包括儿童肿瘤。我们的发现为CHD基因家族的功能和机制提供了新的见解，尤其是在CHD7和CHD9中。。

IntroductionThe CHD (chromosome domain helicase DNA binding protein) gene family is categorized within the adenosine triphosphate (ATP)-dependent chromatin remodeler family, overseeing chromatin remodeling, as indicated by its nomenclature. This family comprises ATP-dependent chromatin remodelers that play indispensable roles in diverse developmental processes.

引言CHD（染色体结构域解旋酶DNA结合蛋白）基因家族被归类为三磷酸腺苷（ATP）依赖性染色质重塑家族，监督染色质重塑，如其命名法所示。该家族包括ATP依赖性染色质重塑剂，它们在不同的发育过程中起着不可或缺的作用。

ATP-dependent chromatin remodeling complexes fall into four subfamilies: switching/sucrose nonfermenting (SWI-SNF), imitation switch (ISWI), CHD, and inositol-requiring 80 (INO80). These subfamilies share a conserved ATPase-containing domain, utilizing ATP hydrolysis to modulate histone-DNA interactions, thereby contributing significantly to organ development and cancer pathogenesis1.

ATP依赖的染色质重塑复合物分为四个亚家族：开关/蔗糖非发酵（SWI-SNF），模拟开关（ISWI），CHD和肌醇需要80（INO80）。这些亚家族共享一个保守的含ATPase的结构域，利用ATP水解来调节组蛋白-DNA相互作用，从而对器官发育和癌症发病机制做出重大贡献1。

The CHD gene family exerts its functional impact by binding to chromatin, influencing transcription activation, and modulating the epigenome through chromatin remodeling processes.While substantial investigations have been conducted on the CHD gene family across diverse cancer types, a comprehensive pan-cancer analysis of the entire CHD gene family is lacking.

CHD基因家族通过与染色质结合，影响转录激活以及通过染色质重塑过程调节表观基因组来发挥其功能影响。尽管已经对不同癌症类型的冠心病基因家族进行了大量研究，但缺乏对整个冠心病基因家族的全面泛癌分析。

Despite the considerable volume of recent cancer studies, the mechanisms by which the CHD gene family influences tumorigenesis and progression, particularly for newly discovered members, remained insufficiently elucidated. For instance, CHD1, identified in 1993, plays crucial roles in various tumors, notably prostate and breast cancers2,3,4.

尽管最近进行了大量的癌症研究，但CHD基因家族影响肿瘤发生和发展的机制，特别是对于新发现的成员，仍未得到充分阐明。例如，1993年发现的CHD1在各种肿瘤中起着至关重要的作用，尤其是前列腺癌和乳腺癌2,3,4。

In contrast, CHD9, reported since 2005, has received limited attention regarding its functions in cancer5. Moreover, the mechanisms of the CHD family are diverse, encompassing distinct cell fates and signal pathways. For example, CHD1 in ovarian cancer interacts with miR-30a-5p, inhibiting the Wnt/β-catenin signaling pathway6.

相比之下，自2005年以来报道的CHD9在癌症中的功能受到的关注有限5。此外，冠心病家族的机制多种多样，包括不同的细胞命运和信号通路。例如，卵巢癌中的CHD1与miR-30a-5p相互作用，抑制Wnt/β-连环蛋白信号通路6。

CHD4 promote.

CHD4升级。

Pan-cancer expression profiles of CHD gene familyInitially, an exhaustive analysis of the expression levels of the CHD gene family was conducted across all 33 cancers within TCGA (The Cancer Genome Atlas) database in comparison to control samples. Gene expression data and DEGs (Differentially Expressed Genes) between cancers and normal tissues were shown using the parameter of log2FC > 1, q value cut-off = 0.01 with ANOVA method.

。使用ANOVA方法，使用log2FC>1，q值截止值=0.01的参数显示癌症和正常组织之间的基因表达数据和DEG（差异表达基因）。

Strikingly, among these cancers, the expression of CHD5 exhibited a very low level (Figure S1A). Further scrutiny focused on cancer types with more than five normal controls in TCGA (Figure S1B-J). Utilizing the GEPIA2 tools, which merges normal controls from TCGA and the GTEx database as its input controls, generated preferable gene expression data for the CHD gene family (Fig. 1).

。进一步的审查集中在TCGA中有五个以上正常对照的癌症类型（图S1B-J）。利用GEPIA2工具，将TCGA的正常对照和GTEx数据库合并为其输入对照，为CHD基因家族生成了更好的基因表达数据（图1）。

In-depth examination revealed distinctive expression patterns for each member. For instance, CHD1 showed significant up-regulation in THYM (Thymoma) but down-regulation in LUSC (Lung Squamous Cell Carcinoma), OV (Ovarian Cancer), TGCT (Testicular Cancer), UCEC (Uterine Corpus Endometrial Cancer) and UCS (Uterine Carcinosarcoma) (Fig. 1a).

深入检查发现每个成员都有独特的表达模式。例如，CHD1在胸腺（胸腺瘤）中显示出显着的上调，但在LUSC（肺鳞状细胞癌），OV（卵巢癌），TGCT（睾丸癌），UCEC（子宫体子宫内膜癌）和UCS（子宫癌）中显示出下调肉瘤）（图1a）。

Similarly, CHD2 displayed parallel trends, being up-regulated in THYM and down-regulated in LUSC, OV, SKCM (Melanoma), UCEC and UCS (Fig. 1b). CHD3 exhibited up-regulation in LAML (Acute Myeloid Leukemia), PAAD (Pancreatic Cancer) and THYM, contrasted by down-regulation in CESC (Cervical Cancer), COAD (Colon Cancer), GBM (Glioblastoma), KICH (Kidney Chromophobe), OV, READ (Rectal Cancer), TGCT, THCA (Thyroid Cancer), UCEC and UCS (Fig. 1c).

同样，CHD2显示出平行的趋势，在胸腺中上调，在LUSC，OV，SKCM（黑色素瘤），UCEC和UCS中下调（图1b）。CHD3在LAML（急性骨髓性白血病），PAAD（胰腺癌）和THYM中表现出上调，而在CESC（宫颈癌），COAD（结肠癌），GBM（胶质母细胞瘤），KICH（肾嫌色细胞），OV，READ（直肠癌），TGCT，THCA（甲状腺癌），UCEC和UCS中则下调（图1c）。

CHD4, conversely, demonstrated significant up-regulation in DLBC (Large B-cell Lymphoma), GBM, LGG (Lower Grade Glioma), PAAD and THYM (Fig. 1d). Noteworthy was the down-regulation of CHD5 in GB.

相反，CHD4在DLBC（大B细胞淋巴瘤），GBM，LGG（低级胶质瘤），PAAD和胸腺中表现出显着的上调（图1d）。值得注意的是GB中CHD5的下调。

PPI network was generated with STRING database and modified by Cytoscape software (version 3.9.1). The confidence score cutoff was set to 0.4 and the top 100 proteins interacted with CHD7 or CHD9 were chosen to intersect with DEGs (fold changes > 2 and P value < 0.01) downloaded from GEPIA2 in LAML, UCEC and UCS, respectively (Table S1).

PPI网络由STRING数据库生成，并由Cytoscape软件（版本3.9.1）修改。置信度得分截止值设置为0.4，选择与CHD7或CHD9相互作用的前100个蛋白质与分别从LAML，UCEC和UCS中的GEPIA2下载的DEG相交（倍数变化>2和P值<0.01）（表S1）。

Up-regulated and down-regulated intersecting DEGs in above cancers were calculated respectively (Table S2). The intersecting DEGs were shown in Venn diagram as well and used to perform GO analysis.Gene Ontology (GO) analysis of intersecting genesGene ontology analysis was performed by R package “clusterProfiler” (version 4.2.1) with identified DEGs from Venn diagram.

分别计算上述癌症中上调和下调的交叉DEG（表S2）。相交的DEG也显示在维恩图中，并用于执行GO分析。交叉基因的基因本体论（GO）分析基因本体论分析由R软件包“clusterProfiler”（版本4.2.1）进行，并从维恩图中识别出DEG。

The adjusted P value < 0.01 was thought to be significant. Biological process (BP), cellular component (CC) and molecular function (MF) sub-ontology were all enriched. Up-regulated DEGs and down-regulated DEGs were enriched separately..

调整后的P值<0.01被认为是显着的。生物过程（BP），细胞成分（CC）和分子功能（MF）子本体都得到了丰富。上调的DEG和下调的DEG分别富集。。

Data availability

数据可用性

All the data used in this paper were downloaded from GDC TCGA database and GDC TARGET database (https://xenabrowser.net/datapages) 36.

本文使用的所有数据均从GDC TCGA数据库和GDC TARGET数据库下载(https://xenabrowser.net/datapages)36页。

AbbreviationsACC:

缩写ACC：

Adrenocortical carcinoma

肾上腺皮质癌

BLCA:

BLCA：

Bladder Urothelial Carcinoma

膀胱尿路上皮癌

BRCA:

BRCA：

Breast invasive carcinoma

乳腺浸润癌

CESC:

CESC：

Cervical squamous cell carcinoma and endocervical adenocarcinoma

宫颈鳞状细胞癌和宫颈腺癌

CHOL:

乔尔：

Cholangio carcinoma

COAD:

COAD：

Colon adenocarcinoma

结肠腺癌

DLBC:

DLBC：

Lymphoid Neoplasm Diffuse Large B-cell Lymphoma

淋巴肿瘤弥漫性大B细胞淋巴瘤

ESCA:

ESCA：

Esophageal carcinoma

食管癌

GBM:

GBM：

Glioblastoma multiforme

多形性胶质母细胞瘤

HNSC:

HNSC：

Head and Neck squamous cell carcinoma

头颈部鳞状细胞癌

KICH:

基奇：

Kidney Chromophobe

肾嫌色细胞

KIRC:

柯克：

Kidney renal clear cell carcinoma

肾透明细胞癌

KIRP:

唧唧：

Kidney renal papillary cell carcinoma

肾乳头状细胞癌

LAML:

拉姆尔：

Acute Myeloid Leukemia

急性骨髓性白血病

LGG:

LGG：

Brain Lower Grade Glioma

脑低级别胶质瘤

LIHC:

LIHC公司：

Liver hepatocellular carcinoma

肝细胞肝癌

LUAD:

鲁德：

Lung adenocarcinoma

肺腺癌

LUSC:

LUSC：

Lung squamous cell carcinoma

肺鳞状细胞癌

MESO:

中观：

Mesothelioma

间皮瘤

OV:

OV：

Ovarian serous cystadenocarcinoma

卵巢浆液性囊腺癌

PAAD:

路径：

Pancreatic adenocarcinoma

胰腺癌

PCPG:

PCPG：

Pheochromocytoma and Paraganglioma

嗜铬细胞瘤和副神经节瘤

PRAD:

PRAD：

Prostate adenocarcinoma

前列腺腺癌

READ:

阅读：

Rectum adenocarcinoma

直肠腺癌

SARC:

SARC公司：

Sarcoma

肉瘤

SKCM:

SKCM：

Skin cutaneous melanoma

皮肤黑色素瘤

STAD:

STAD：

Stomach adenocarcinoma

胃腺癌

TGCT:

TGCT：

Testicular germ cell tumors

睾丸生殖细胞肿瘤

THCA:

THCA：

Thyroid carcinoma

甲状腺癌

THYM:

百里香：

Thymoma

胸腺瘤

UCEC:

UCEC：

Uterine Corpus Endometrial Carcinoma

子宫体子宫内膜癌

UCS:

UCS：

Uterine Carcinosarcoma

子宫癌肉瘤

UVM:

UVM:

Uveal melanoma

葡萄膜黑色素瘤

ALL-P3:

ALL-P3：

Acute lymphoblastic leukemia-Phase 3

急性淋巴细胞白血病3期

AML:

反洗钱：

Acute Myeloid Leukemia

急性骨髓性白血病

CCSK:

CCSK：

Clear cell sarcoma of the kidney

肾透明细胞肉瘤

NBL:

NBL：

Neuroblastoma

神经母细胞瘤

OS:

操作系统：

Osteosarcoma

骨肉瘤

RT:

室温：

Rhabdoid tumor

横纹肌样瘤

WT:

重量：

Wilms tumor

肾母细胞瘤

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Download referencesAcknowledgementsWe thank Dr. Chuantao Fang for technical support of R scripts and Dr. Weijun Feng for advice of manuscripts. This work was supported by the Grant from National Natural Science Foundation of China (No. 82301840 to Jie Cheng).Author informationAuthor notesThese authors contributed equally: Yujia Lu, Jiebang Jiang and Zhihong He.Authors and AffiliationsShanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaYujia LuJiangsu Province Engineering Research Center of Cardiovascular Drugs Targeting, School of Life Sciences, Jiangsu Normal University, Xuzhou, Jiangsu, ChinaJiebang JiangDepartment of Obstetrics and Gynecology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaZhihong He & Zhouzhou BaoShanghai Key Laboratory of Gynecologic Oncology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaZhouzhou BaoDepartment of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, ChinaXin ChenCenter for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai, ChinaXin ChenInstitute of Gastrointestinal Surgery and Translational Medicine, Tongji University, School of Medicine, Shanghai, ChinaXin ChenCenter for Reproductive Medicine, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaJie ChengShanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, ChinaJie ChengAuthorsYujia LuView author publicationsYou can also search for this author in.

下载参考文献致谢我们感谢方川涛博士对R脚本的技术支持，以及冯伟军博士对稿件的建议。这项工作得到了国家自然科学基金（第82301840号给Jie Cheng）的资助。作者信息作者注意到这些作者做出了同样的贡献：陆玉嘉，蒋洁邦和何志红。，上海交通大学医学院仁济医院，上海，中国上海，上海辅助生殖与生殖遗传学重点实验室，上海，中国上海，Chengjie ChengAuthorsYujia LuView作者出版物您也可以在中搜索这位作者。

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PubMed Google ScholarContributionsConceptualization, Y.L. and J.C.; methodology, Y.L., J.J and Z.H.; software, X.C.; validation, J.J. and X.C; formal analysis, Z.H.; investigation, Y.L.; resources, Z.H.; data curation, Y.L.; writing—original draft preparation, Y.L.; writing—review and editing, All authors; visualization, Z.H; supervision, Z.B, X.C and J.C.; project administration, Z.B, X.C and J.C.; funding acquisition, J.C.

PubMed谷歌学术贡献概念化，Y.L.和J.C。；方法论，Y.L.，J.J和Z.H。；软件，X.C。；验证，J.J.和X.C；形式分析，Z.H。；调查，Y.L。；资源，Z.H。；数据管理，Y.L。；撰写原稿准备，Y.L。；写作评论和编辑，所有作者；可视化，Z.H；监督，Z.B，X.C和J.C。；项目管理，Z.B，X.C和J.C。；。

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Reprints and permissionsAbout this articleCite this articleLu, Y., Jiang, J., He, Z. et al. Molecular characteristics and oncogenic role of CHD family genes: a pan-cancer analysis based on bioinformatic and biological analysis.

转载和许可本文引用本文Lu，Y.，Jiang，J.，He，Z。等人。CHD家族基因的分子特征和致癌作用：基于生物信息学和生物学分析的泛癌分析。

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Keywords

关键词

CHD gene familyPan-cancerKnock downEpigenomeChildhood tumor

CHD基因家族癌基因敲除表观遗传机制良性肿瘤

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