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转录组学与功能验证揭示PAQR3/P6-55作为结肠癌潜在治疗靶点

Transcriptomic and Functional Validation Reveals PAQR3/P6-55 as Potential Therapeutic Targets in Colon Cancer.

作者信息

You Xue, Gai Yikuo, Wang Ziyun, Wang Yanqi, Ye Jingran, Cao Yujia, Zhang Hengshuo, Zhang Ziyi, Feng Ying

机构信息

Lin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, 133 Hehua Road, Jining 272067, China.

College of Clinical Medicine, Jining Medical University, Jining 272067, China.

出版信息

Biology (Basel). 2025 Jun 27;14(7):780. doi: 10.3390/biology14070780.

DOI:10.3390/biology14070780
PMID:40723340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12292340/
Abstract

Colon cancer is one of the leading malignant tumors worldwide, and the membrane protein PAQR3 has been identified as a tumor suppressor in multiple cancers. Notably, the peptide synthesized from 6 to 55 amino acids at the N-terminal of PAQR3 (P6-55) has been shown to effectively inhibit the growth of gastric cancer cells. This study aims to elucidate the mechanism of PAQR3 and explore its therapeutic potential in colon cancer. CCK8 cell viability assays, colony formation assays, and transwell migration assays were employed to systematically assess the inhibitory effects of PAQR3 on the proliferation and migration of colon cancer cells. Furthermore, we confirmed that P6-55 exhibits functional similarities to PAQR3, effectively inhibiting the growth of colon cancer in vitro and in vivo. RNA sequencing revealed that PAQR3 suppresses tumor growth via the PI3K-AKT signaling pathway, providing a strong theoretical foundation for therapeutic strategies targeting PAQR3/P6-55. In conclusion, our findings highlight the therapeutic potential of PAQR3/P6-55 as novel colon cancer inhibitors.

摘要

结肠癌是全球主要的恶性肿瘤之一，膜蛋白PAQR3已被确定为多种癌症中的肿瘤抑制因子。值得注意的是，从PAQR3 N端第6至55个氨基酸合成的肽（P6-55）已被证明能有效抑制胃癌细胞的生长。本研究旨在阐明PAQR3的作用机制，并探索其在结肠癌中的治疗潜力。采用CCK8细胞活力测定、集落形成测定和Transwell迁移测定来系统评估PAQR3对结肠癌细胞增殖和迁移的抑制作用。此外，我们证实P6-55与PAQR3具有功能相似性，能在体外和体内有效抑制结肠癌的生长。RNA测序显示，PAQR3通过PI3K-AKT信号通路抑制肿瘤生长，为靶向PAQR3/P6-55的治疗策略提供了有力的理论基础。总之，我们的研究结果突出了PAQR3/P6-55作为新型结肠癌抑制剂的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/ee476bc286f6/biology-14-00780-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/03dd613415aa/biology-14-00780-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/2c3c7619a5fe/biology-14-00780-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/a3c7b835e9e9/biology-14-00780-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/2c9cfeafddbc/biology-14-00780-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/af346c5d4c45/biology-14-00780-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/ee476bc286f6/biology-14-00780-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/03dd613415aa/biology-14-00780-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/2c3c7619a5fe/biology-14-00780-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/a3c7b835e9e9/biology-14-00780-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/2c9cfeafddbc/biology-14-00780-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/af346c5d4c45/biology-14-00780-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df06/12292340/ee476bc286f6/biology-14-00780-g006.jpg

相似文献

[1]
Transcriptomic and Functional Validation Reveals PAQR3/P6-55 as Potential Therapeutic Targets in Colon Cancer.

Biology (Basel). 2025-6-27

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[4]
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[5]
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[6]
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[7]
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[8]
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J Ethnopharmacol. 2025-7-3

[9]
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[10]
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Transl Cancer Res. 2025-5-30

本文引用的文献

[1]
L3MBTL3 and STAT3 collaboratively upregulate SNAIL expression to promote metastasis in female breast cancer.

Nat Commun. 2025-1-2

[2]
ERBB3 targeting: A promising approach to overcoming cancer therapeutic resistance.

Cancer Lett. 2024-9-1

[3]
Identification of ASMTL-AS1 and LINC02604 lncRNAs as novel biomarkers for diagnosis of colorectal cancer.

Int J Colorectal Dis. 2024-7-19

[4]
The PI3K/Akt Pathway and Glucose Metabolism: A Dangerous Liaison in Cancer.

Int J Biol Sci. 2024

[5]
Advancements in combining targeted therapy and immunotherapy for colorectal cancer.

Trends Cancer. 2024-7

[6]
Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries.

CA Cancer J Clin. 2024

[7]
CircHAS2 activates CCNE2 to promote cell proliferation and sensitizes the response of colorectal cancer to anlotinib.

Mol Cancer. 2024-3-21

[8]
Wnt/β-catenin-driven EMT regulation in human cancers.

Cell Mol Life Sci. 2024-2-9

[9]
Gut microbial metabolite facilitates colorectal cancer development via ferroptosis inhibition.

Nat Cell Biol. 2024-1

[10]
Therapeutic cancer vaccines: advancements, challenges, and prospects.

Signal Transduct Target Ther. 2023-12-13

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