Dataset Information

Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma.

ABSTRACT:

Background

Our previous study showed that Cyclin B2 (CCNB2) is closely related to the occurrence and progression of hepatocellular carcinoma (HCC).

Aim of the study

This study aimed to clarify the effect of CCNB2 gene silencing on tumorigenesis in nude mice and to detect the potential mechanism.

Methods

The effect of CCNB2 on HCC was tested in vivo. The downstream target genes of CCNB2 were predicted by proteomics and confirmed by western blot assay. The regulatory functions of CCNB2 in the proliferation and migration of HCC cells were determined through functional recovery experiments. The expression of the downstream target genes of CCNB2 was detected by immunohistochemistry.

Results

Knockdown of CCNB2 decreased tumour formation rate and tumour volume and weight and inhibited tumour proliferation. A total of 130 differentially expressed proteins were detected by proteomics, and Jagged 1 (JAG1) was predicted as the potential downstream target of CCNB2. Western blot assay revealed that CCNB2 and JAG1 expression was significantly correlated in HCC cells. The results of functional recovery experiments suggested that CCNB2 knockdown weakened the proliferation and migration ability of HCC cells, while JAG1 overexpression restored this ability of HCC cells that was weakened by CCNB2 knockdown. Immunohistochemistry showed that JAG1 expression was higher in HCC tissues than in paracancerous tissues and was related to tumour size and number and tumour thrombus formation.

Conclusions

The proliferation of HCC cells in vivo was inhibited by CCNB2 knockdown. CCNB2 may accelerate the proliferation and metastasis of HCC cells by increasing JAG1 expression.

SUBMITTER: Xiao Y

PROVIDER: S-EPMC9004552 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Publications

Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma.

Xiao Yening Y Ma Jiamei J Guo Chunliu C Liu Danni D Pan Jing J Huang Xiaoxi X

Aging 20220329 6

<h4>Background</h4>Our previous study showed that Cyclin B2 (<i>CCNB2</i>) is closely related to the occurrence and progression of hepatocellular carcinoma (HCC).<h4>Aim of the study</h4>This study aimed to clarify the effect of <i>CCNB2</i> gene silencing on tumorigenesis in nude mice and to detect the potential mechanism.<h4>Methods</h4>The effect of <i>CCNB2</i> on HCC was tested <i>in vivo</i>. The downstream target genes of CCNB2 were predicted by proteomics and confirmed by western blot as ...[more]

PMID: 35349480

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Project description:BackgroundInterleukin-33 (IL-33) is an effective inducer of pro-inflammatory cytokines regulating innate and adaptive immunity. Inflammation could be a double-edged sword, promoting or inhibiting tumour growth. To date, the roles and mechanisms of IL-33 in tumours remain controversial. Here, we examined the effect of exogenous IL-33 on the biological characteristics of hepatocellular carcinoma (HCC) and the possible mechanism of action.MethodsIn this study, IL-33 expression in the tissues of 69 HCC patients was detected and its relationship with prognosis was evaluated. After establishing a mouse HCC model and IL-33 treatment operation, the infiltration of splenic myeloid-derived suppressor (MDSCs), dendritic (DCs), regulatory T, and natural killer (NK) cells was detected by flow cytometry analysis, and the vascular density of the tumour tissues was detected by immunohistochemistry to reveal the mechanism of IL-33 in HCC proliferation. Finally, the Cancer Genome Atlas database was used to analyse Gene Ontology terms the and Kyoto Encyclopaedia of Genes and Genomes pathway. Moreover, the chi-square test, two-tailed unpaired Student's t-test, and multiple t-tests were performed using SPSS version 23.0 and GraphPad Prism 8.0 software.ResultsThe IL-33 expression level was negatively correlated with the overall survival of HCC patients, suggesting its potential clinical significance in the prognosis of HCC. We found that systemic IL-33 administration significantly promoted the tumour size in vivo. Furthermore, the IL-33-treated mice presented decreased frequencies of tumouricidal NK and CD69+ CD8+ T cells. After IL-33 treatment, the incidence of monocytic MDSCs and conventional DCs increased, while that of granulocytic MDSCs decreased. Moreover, IL-33 promoted the formation of intracellular neovascularization. Therefore, IL-33 accelerated HCC progression by increasing the accumulation of immunosuppressive cells and neovascularization formation. Finally, we found that the transcription of IL-33 was closely related to the PI3K-Akt and MAPK pathways in Gene Set Enrichment Analysis plots, which were involved in the tumourigenesis and pathogenesis of HCC.ConclusionsTaken together, IL-33 may be a key tumour promoter of HCC proliferation and tumourigenicity, an important mediator, and a potential therapeutic target for regulating HCC progression.

Dataset Information

Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma.

Background

Aim of the study

Methods

Results

Conclusions

Publications

Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma.

Similar Datasets

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