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UPK1B在胃癌中的作用：多组学分析与实验验证

The role of UPK1B in gastric cancer: multi-omics analysis and experimental validation.

作者信息

Zhu Haixing, Jiang Wen, Zhang Qian, Yu Changjun

机构信息

Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui Province, People's Republic of China.

出版信息

Discov Oncol. 2025 Apr 7;16(1):476. doi: 10.1007/s12672-025-02263-2.

DOI:10.1007/s12672-025-02263-2
PMID:40189715
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11973043/
Abstract

BACKGROUND

UPK1B has been implicated in various cancers; however, its mechanism of action in gastric cancer remains elusive.

METHODS

We utilized transcriptional data and clinical information, and mutation profiles from The Cancer Genome Atlas (TCGA) database to analyze UPK1B's expression and clinical relevance. Biological enrichment, immune microenvironment characterization, and drug sensitivity analyses were conducted. Functional assays, including proliferation, migration, invasion, and in vivo metastasis models, were used to validate UPK1B's role in gastric cancer.

RESULTS

UPK1B was significantly upregulated in gastric cancer and correlated with worse clinical outcomes, including advanced stages and reduced survival rates. Biological enrichment analysis revealed its involvement in cancer-related pathways such as DNA replication and immune regulation. UPK1B was negatively correlated with NK cells and M1 macrophages, indicating its role in immune evasion. Functional experiments demonstrated that knockdown of UPK1B significantly suppressed gastric cancer cell proliferation, invasion, and migration in vitro and reduced pulmonary metastases in vivo. Drug sensitivity analysis suggested that high UPK1B expression was associated with increased sensitivity to lapatinib and resistance to cisplatin.

CONCLUSIONS

UPK1B promotes tumor progression and modulates the immune microenvironment in gastric cancer, making it a potential therapeutic target for future research and clinical applications.

摘要

背景

UPK1B已被证明与多种癌症有关；然而，其在胃癌中的作用机制仍不清楚。

方法

我们利用来自癌症基因组图谱（TCGA）数据库的转录数据、临床信息和突变谱，分析UPK1B的表达及其临床相关性。进行了生物富集、免疫微环境特征分析和药物敏感性分析。采用包括增殖、迁移、侵袭和体内转移模型在内的功能试验，以验证UPK1B在胃癌中的作用。

结果

UPK1B在胃癌中显著上调，且与较差的临床结果相关，包括晚期和较低的生存率。生物富集分析显示其参与了DNA复制和免疫调节等癌症相关途径。UPK1B与自然杀伤细胞和M1巨噬细胞呈负相关，表明其在免疫逃逸中的作用。功能实验表明，敲低UPK1B可显著抑制胃癌细胞的体外增殖、侵袭和迁移，并减少体内肺转移。药物敏感性分析表明，高表达的UPK1B与对拉帕替尼的敏感性增加和顺铂耐药有关。

结论

UPK1B促进胃癌肿瘤进展并调节免疫微环境，使其成为未来研究和临床应用的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/45285e82f320/12672_2025_2263_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/2c865e93e37b/12672_2025_2263_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/4a211a524fec/12672_2025_2263_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/5b4f77059e40/12672_2025_2263_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/da7292e86669/12672_2025_2263_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/43306f0005cf/12672_2025_2263_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/94f6242b2613/12672_2025_2263_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/45285e82f320/12672_2025_2263_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/2c865e93e37b/12672_2025_2263_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/4a211a524fec/12672_2025_2263_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/5b4f77059e40/12672_2025_2263_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/da7292e86669/12672_2025_2263_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/43306f0005cf/12672_2025_2263_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/94f6242b2613/12672_2025_2263_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ae/11973043/45285e82f320/12672_2025_2263_Fig7_HTML.jpg

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