2. Academic Validation
  3. NVS-ZP7-4 inhibits hepatocellular carcinoma tumorigenesis and promotes apoptosis via PI3K/AKT signaling

NVS-ZP7-4 inhibits hepatocellular carcinoma tumorigenesis and promotes apoptosis via PI3K/AKT signaling

  • Sci Rep. 2023 Jul 21;13(1):11795. doi: 10.1038/s41598-023-38596-7.
Qing Tong # 1,  Dong Yan # 1,  Yan Cao 1,  Xiaogang Dong 1,  Yimamumaimaitijiang Abula 1,  Huan Yang 1,  Panpan Kong 1,  Mingyu Yi 2 3
Affiliations

Affiliations

  • 1 Department of Hepatopancreatobiliary Surgery, Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
  • 2 Department of Hepatopancreatobiliary Surgery, Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China. [email protected].
  • 3 Department of Anesthesiology, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Changsha City, 410000, Hunan, China. [email protected].
  • # Contributed equally.
PMID: 37479837 DOI: 10.1038/s41598-023-38596-7
Abstract

NVS-ZP7-4 was identified as a novel chemical reagent targeting the zinc input protein ZIP7, which accounts for the zinc surge from the apparatus to the cytoplasm. Since zinc dysregulation is related to multiple diseases, in this study, we aimed to identify the anti-tumor effects of NVS-ZP7-4 and explore the molecular mechanisms of NVS-ZP7-4 in hepatocellular carcinoma (HCC) progression. We found that NVS-ZP7-4 inhibited cell viability, caused cell cycle arrest, induced Apoptosis, and inhibited the proliferation, migration, and invasion of HCCLM3 and Huh7 cells. We further investigated the inhibited activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway was involved in the antitumor effect of NVS-ZP7-4 in HCC. Furthermore, NVS-ZP7-4 inhibited HCC tumor growth in vivo. The present study demonstrated that NVS-ZP7-4 is a promising therapeutic target for HCC by regulating PI3K/Akt signaling.

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