CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation

Du, Youwen1; Pan, Linxin1; Zhang, Wenchen1; Wei, Shuangbiao1; Fan, Xu1; Zhang, Na1; Wei, Pengjun2; Chen, Xiaoqian3; Qiao, Zhi1; Xie, Li4

2024-09-01

10.2174/0115680096332450240827070033

CURRENT CANCER DRUG TARGETS   影响因子和分区

1568-0096

1873-5576

Introduction: Hepatocellular carcinoma (HCC) is a global health problem with increasing morbidity and mortality, and exploring the diagnosis and treatment of HCC at the gene level is a research hotspot in recent years. As the rate-limiting enzyme of carnosine hydrolysis, CNDP1 participate in the progress of many diseases, but its function has not been revealed in HCC absolutely. Methods: This paper firstly screened differentially expressed genes from the biochip related to HCC by bioinformatic analysis, and CNDP1 was finally selected for in-depth study. Then the bioinformatics analysis results were validated by detecting the expression of CNDP1 in human HCC samples and hepatoma cell lines. Furthermore, the effect of CNDP1 on the malignant behavior of hepatoma cell lines were detected by MTT colorimetric assay, EdU staining assay, colony formation, wound-healing assay and transwell, and the molecular mechanism has also been preliminarily explored. Results: this paper found that the expression of CNDP1 was decreased significantly in human HCC tissues and cell lines, and its overexpression could significantly suppress cell proliferation, migration and invasion of of hepatoma cell lines. Mechanismly, the GeneMANIA database predicted that CNDP1 could interact with various proteins involved in regulating PI3K-AKT-mTOR signaling pathway. Furthermore, this study showed that CNDP1 overexpression could effectively inhibit the activation of PI3K-AKT-mTOR signaling pathways, more significantly, inhibition of PI3K-AKT-mTOR signaling pathway could disrupt the anti-cancer effect of CNDP1 on HCC. Conclusion: This paper confirm that CNDP1 is expression decreased significantly in HCC, and has potential anti-cancer activity, this discovery will provide a cytological basis for further understanding the biological function of CNDP1 and diagnosis and gene therapy of HCC in the future..

Hepatocellular carcinoma CNDP1, proliferation, PI3K-AKT-mTOR

SCI

英语

其他

Natural Science Foundation of Anhui Province[2108085QH309]

Oncology

Oncology

WOS:001311363300001

BENTHAM SCIENCE PUBL LTD

Web of Science

1.Anhui Med Univ, Sch Life Sci, Hefei, Anhui, Peoples R China
2.Nanjing Med Univ, Dept Microbiol, Nanjing, Jiangsu, Peoples R China
3.Southern Univ Sci & Technol, Sch Life Sci, Shenzhen, Guangdong, Peoples R China
4.Univ Sci & Technol China, Affiliated Hosp Univ Sci & Technol China USTC 1, Dept Ultrasound, Div Life Sci & Med, Hefei, Anhui, Peoples R China

Du, Youwen,Pan, Linxin,Zhang, Wenchen,et al. CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation[J]. CURRENT CANCER DRUG TARGETS,2024.

Du, Youwen.,Pan, Linxin.,Zhang, Wenchen.,Wei, Shuangbiao.,Fan, Xu.,...&Xie, Li.(2024).CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation.CURRENT CANCER DRUG TARGETS.

Du, Youwen,et al."CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation".CURRENT CANCER DRUG TARGETS (2024).