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NAP1L1 interacts with hepatoma-derived growth factor to recruit c-Jun inducing breast cancer growth

Shu Liu^1,2, Yewei Zhang³, Shien Cui^4,5

¹Department of Breast Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550001, Guizhou, People's Republic of China. 3543359430@qq.com.

Cancer Cell International

|November 14, 2021

Abstract

Background:

Breast cancer is a common cancer among women in the world. However, its pathogenesis is still to be determined. The role and molecular mechanism of Nucleosome Assembly Protein 1 Like 1 (NAP1L1) in breast cancer have not been reported. Elucidation of molecular mechanism might provide a novel therapeutic target for breast cancer treatment.

Methods:

A bioinformatics analysis was conducted to determine the differential expression of NAP1L1 in breast cancer and find the potential biomarker that interacts with NAP1L1 and hepatoma-derived growth factor (HDGF). The expression of NAP1L1 in tissues was detected by using immunohistochemistry. Breast cancer cells were transfected with the corresponding lentiviral particles and siRNA. The efficiency of transfection was measured by RT-qPCR and western blotting. Then, MTT, Edu, plate clone formation, and subcutaneous tumorigenesis in nude mice were used to detect the cell proliferation in breast cancer. Furthermore, coimmunoprecipitation (Co-IP) assay and confocal microscopy were performed to explore the detailed molecular mechanism of NAP1L1 in breast cancer.

Results:

In this study, NAP1L1 protein was upregulated based on the Clinical Proteomic Tumor Analysis Consortium (CPTAC) database. Consistent with the prediction, immunohistochemistry staining showed that NAP1L1 protein expression was significantly increased in breast cancer tissues. Its elevated expression was an unfavorable factor for breast cancer clinical progression and poor prognosis. Stably or transiently knocking down NAP1L1 reduced the cell growth in vivo and in vitro via repressing the cell cycle signal in breast cancer. Furthermore, the molecular basis of NAP1L1-induced cell cycle signal was further studied. NAP1L1 interacted with the HDGF, an oncogenic factor for tumors, and the latter subsequently recruited the key oncogenic transcription factor c-Jun, which finally induced the expression of cell cycle promoter Cyclin D1(CCND1) and thus the cell growth of breast cancer.

Conclusions:

Our data demonstrated that NAP1L1 functions as a potential oncogene via interacting with HDGF to recruit c-Jun in breast cancer.

Insights

Nucleosome Assembly Protein 1 Like 1 (NAP1L1) is upregulated in breast cancer, promoting cell growth by interacting with HDGF and c-Jun. Targeting NAP1L1 may offer a new therapeutic strategy for breast cancer.

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Breast cancer pathogenesis remains incompletely understood.
The role of Nucleosome Assembly Protein 1 Like 1 (NAP1L1) in breast cancer is not well-defined.
Identifying novel therapeutic targets is crucial for breast cancer treatment.

Purpose of the Study:

To investigate the differential expression and molecular mechanism of NAP1L1 in breast cancer.
To explore NAP1L1's potential as a biomarker and therapeutic target.

Main Methods:

Bioinformatic analysis and immunohistochemistry to assess NAP1L1 expression.
In vitro and in vivo experiments using cell transfection and tumor xenografts to evaluate cell proliferation.
Co-immunoprecipitation and confocal microscopy to elucidate molecular interactions.

Main Results:

NAP1L1 protein was significantly upregulated in breast cancer tissues, correlating with poor prognosis.
Knockdown of NAP1L1 inhibited breast cancer cell growth both in vitro and in vivo.
NAP1L1 was found to interact with hepatoma-derived growth factor (HDGF) and recruit c-Jun, leading to Cyclin D1 expression and cell cycle promotion.

Conclusions:

NAP1L1 acts as a potential oncogene in breast cancer.
The NAP1L1-HDGF-c-Jun axis drives breast cancer cell proliferation.
NAP1L1 represents a promising therapeutic target for breast cancer.

Read full analysis

Keywords:

Breast cancer C-JUN HDGF NAP1L1 Oncogene

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