Mechanism of PDZK1 in Hepatocellular Carcinoma Complicated with Hyperuricemia.


Journal

Journal of oncology
ISSN: 1687-8450
Titre abrégé: J Oncol
Pays: Egypt
ID NLM: 101496537

Informations de publication

Date de publication:
2022
Historique:
received: 09 08 2022
revised: 27 09 2022
accepted: 11 10 2022
entrez: 24 11 2022
pubmed: 25 11 2022
medline: 25 11 2022
Statut: epublish

Résumé

Hepatocellular carcinoma (HCC) is a kind of primary liver cancer that accounts for more than 90% of primary hepatocellular carcinomas. Hyperuricemia is closely related to the development, recurrence, metastasis, and prognosis of cancer. Previous studies have proved that the serum uric acid level can increase the incidence rate and mortality of malignant tumors. However, the specific pathogenesis remains unstudied. RT-qPCR analysis showed that the mRNA expression of PDZK1 and ABCG2 increased significantly after HCC cells were exposed to different concentrations of soluble uric acid (2.5, 5, 10, 20 mg/dl) for 24 hours. Then, in HCC shRNAs, PDZK1, or over expression PDZK1 were used. CCK8, wound healing, and Transwell assay showed that PDZK1 regulates cell proliferation, invasion, and migration. Flow cytometry results revealed that PDZK1 affects cell apoptosis. Western blot results show that PDZK1 affects the STAT3/C-myc pathway. Then, in vivo tumorigenesis, allopurinol maybe an effective drug to advance: the prognosis of HCC. In our study, RT-qPCR analysis showed that the mRNA expression of PDZK1 and ABCG2 increased significantly after different concentrations of soluble uric acid in HCC. Then, PDZK1 affects the proliferation, migration, and apoptosis of HCC through the STAT3/C-myc pathway. Hyperuricemia response affects the expression of PDZK1; PDZK1 affects the proliferation, migration, and apoptosis through the STAT3/C-myc pathway in hepatocellular carcinoma. It is suggested that PDZK1 maybe closely related to the occurrence, development, and prognosis of HCC and allopurinol maybe have potential anticancer effects.

Sections du résumé

Background UNASSIGNED
Hepatocellular carcinoma (HCC) is a kind of primary liver cancer that accounts for more than 90% of primary hepatocellular carcinomas. Hyperuricemia is closely related to the development, recurrence, metastasis, and prognosis of cancer. Previous studies have proved that the serum uric acid level can increase the incidence rate and mortality of malignant tumors. However, the specific pathogenesis remains unstudied.
Methods UNASSIGNED
RT-qPCR analysis showed that the mRNA expression of PDZK1 and ABCG2 increased significantly after HCC cells were exposed to different concentrations of soluble uric acid (2.5, 5, 10, 20 mg/dl) for 24 hours. Then, in HCC shRNAs, PDZK1, or over expression PDZK1 were used. CCK8, wound healing, and Transwell assay showed that PDZK1 regulates cell proliferation, invasion, and migration. Flow cytometry results revealed that PDZK1 affects cell apoptosis. Western blot results show that PDZK1 affects the STAT3/C-myc pathway. Then, in vivo tumorigenesis, allopurinol maybe an effective drug to advance: the prognosis of HCC.
Results UNASSIGNED
In our study, RT-qPCR analysis showed that the mRNA expression of PDZK1 and ABCG2 increased significantly after different concentrations of soluble uric acid in HCC. Then, PDZK1 affects the proliferation, migration, and apoptosis of HCC through the STAT3/C-myc pathway.
Conclusions UNASSIGNED
Hyperuricemia response affects the expression of PDZK1; PDZK1 affects the proliferation, migration, and apoptosis through the STAT3/C-myc pathway in hepatocellular carcinoma. It is suggested that PDZK1 maybe closely related to the occurrence, development, and prognosis of HCC and allopurinol maybe have potential anticancer effects.

Identifiants

pubmed: 36420358
doi: 10.1155/2022/1403454
pmc: PMC9678461
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1403454

Informations de copyright

Copyright © 2022 Linqi Guo et al.

Déclaration de conflit d'intérêts

The authors declare that they have no conflicts of interest.

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Auteurs

Linqi Guo (L)

School of Basic Medicine Jiamusi University, Jiamusi 154000, China.
Department of General Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi 154000, China.

Wenda Jiang (W)

Department of General Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi 154000, China.

Lingli Quan (L)

Pulmonary and Critical Care Medicine 1, The Affiliated Zhuzhou Hospital Xiangya Medical College CSU, Zhuzhou 412000, China.

Xinli Teng (X)

Medical Oncology, The Tumor Hospital of Jiamusi, Jiamusi 154000, China.

Jing Zhao (J)

School of Basic Medicine Jiamusi University, Jiamusi 154000, China.
Department of General Surgery, The First Affiliated Hospital of Jiamusi University, Jiamusi 154000, China.

Hongbin Qiu (H)

School of Basic Medicine Jiamusi University, Jiamusi 154000, China.
School of Public Health Jiamusi University, Jiamusi 154000, China.

Classifications MeSH