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Transcriptomic and Functional Validation Reveals PAQR3/P6-55 as Potential Therapeutic Targets in Colon Cancer
by
, ,
Xue You
1,*
,
Yikuo Gai
2,
Ziyun Wang
3,
Yanqi Wang
2,
Jingran Ye
2,
Yujia Cao
2,
Hengshuo Zhang
2,
Ziyi Zhang
3 and
Ying Feng
1,* 1
Lin He’s Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, 133 Hehua Road, Jining 272067, China
2
College of Clinical Medicine, Jining Medical University, Jining 272067, China
3
College of Medical Imaging and Laboratory, Jining Medical University, Jining 272067, China
*
Authors to whom correspondence should be addressed.
Biology 2025, 14(7), 780; https://doi.org/10.3390/biology14070780 (registering DOI)
Submission received: 1 May 2025
/
Revised: 10 June 2025
/
Accepted: 25 June 2025
/
Published: 27 June 2025
Simple Summary
This study explores the roles and therapeutic potential of Progestin and adipoQ receptor 3 (PAQR3) in colon cancer. It was found that the peptide segment P6-55, synthesized from 6 to 55 amino acids at the N-terminus of PAQR3, functions similarly to PAQR3 and effectively inhibits the growth of colon cancer both in vitro and in vivo. RNA sequencing indicated that PAQR3 suppresses tumor growth via the PI3K-AKT signaling pathway, providing a theoretical basis for therapeutic strategies targeting PAQR3/P6-55.
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.
Keywords:
PAQR3; P6-55; PI3K-AKT; colon cancer
