ZNF655 promotes the progression of hepatocellular carcinoma through PSMB8

Author:

Fan Shasha1,Liu Yu2,Lin Zhenhai34,Zhang Yongfa34ORCID,Zhang Ning34,Zhao Yiming34,Zhou Jiaming34,Mao Anrong34,Wang Longrong34,Feng Yun34,He Xigan34,Wang Lu34,Pan Qi34ORCID

Affiliation:

1. Department of Oncology The First Affiliated Hospital of Hunan Normal University, Hunan Provincial People's Hospital, Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Hunan Normal University Changsha Hunan China

2. Department of Pathology Hunan Provincial People's Hospital Changsha Hunan China

3. Department of Hepatic Surgery Fudan University Shanghai Cancer Center, Fudan University Shanghai China

4. Department of Oncology Shanghai Medical College, Fudan University Shanghai China

Abstract

AbstractHepatocellular carcinoma (HCC) is a type of liver cancer that is associated with high mortality rates. This study aims to investigate the role of ZNF655, a member of the zinc finger protein family, in the development of HCC. Immunohistochemical staining analysis was conducted to evaluate the expression of ZNF655 in HCC patient samples. Lentivirus‐mediated ZNF655 knockdown was established in HCC cell lines (BEL‐7402 and HCCLM3). The effects of ZNF655 on different aspects of HCC cell behavior such as proliferation, apoptosis, cycle, migration and tumor formation were examined. Downstream targets of ZNF655 in HCC were identified and verified through loss/gain‐of‐function experiments. Clinically, ZNF655 expression was elevated in HCC and increased with the severity of the disease. Functionally, inhibition of ZNF655 expression reduced the progression of HCC cells by decreasing proliferation, causing apoptosis, arresting cell cycle retention in G2, suppressing migration, and attenuating tumor formation in mice. Mechanistically, the proteasome subunit beta type‐8 (PSMB8) was found to be co‐expressed with ZNF655 in HCC, and PSMB8 knockdown weakened the promotion of ZNF655 overexpression on HCC. In summary, these findings suggest that ZNF655 promotes the progression of HCC through PSMB8, and inhibition of its expression may be a promising therapeutic target for HCC.

Funder

Natural Science Foundation of Shanghai

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cell Biology,General Medicine

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