Dataset Information

Pan-cancer and multi-omics analyses reveal the diagnostic and prognostic value of BAZ2B

ABSTRACT: The BAZ2B gene belongs to the bromodomain gene family. The proteins encoded by members of this gene family are important components of chromatin remodelling complexes and have a potential role in transcriptional activation. However, the biological significance of BAZ2B in pan-cancer is unknown. In this study, we comprehensively analysed the functional characteristics of BAZ2B in human cancers and its role in immune response using The Cancer Genome Atlas (TCGA), Gene Expression Album (GEO), Genotype-Tissue Expression (GTEx) databases, and tools such as TIMER 2.0 and cBioPortal, and found that BAZ2B is down-regulated in certain cancers, and its overexpression is associated with patients’ poor prognosis, such as bladder, breast and endometrial cancers. In addition, we demonstrated for the first time that BAZ2B was under-expressed in breast cancer cells and promoted proliferation, migration and apoptosis of breast cancer cells.

ORGANISM(S): Homo Sapiens

SUBMITTER: Yan Liu

PROVIDER: PXD054319 | iProX | Fri Jul 26 00:00:00 BST 2024

REPOSITORIES: iProX

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Pan-cancer and multi-omics analyses reveal the diagnostic and prognostic value of BAZ2B in cancer.

Guo Jimin J Wang Shuqing S Liu Yan Y Zhang Bin B Zhang Jinghua J Wu Jinghua J Qi Guijie G Shen Zhihao Z Guo Rui R Du Panyan P Zhang Ying Y Zhao Mingjia M Han Liyuan L Zhou Linfeng L Li Yufeng Y Zhao Yating Y

Scientific reports 20260107 1

Bromodomain adjacent to zinc finger domain 2B (BAZ2B) is involved in chromatin remodeling, non-coding RNA regulation, and aging. However, its role in cancer remains unclear. Using multiple databases (TCGA, GEO, GTEx, TIMER2.0, cBioPortal), we found that BAZ2B is downregulated in many cancers, including breast cancer. Low BAZ2B correlates with poor prognosis, immune infiltration, and diagnostic potential, as shown by ROC and Kaplan-Meier analyses. Functionally, BAZ2B knockdown promoted breast can ...[more]

PMID: 41501318

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Project description:Deleted in Liver Cancer-1 (DLC1), a member of the RhoGAP family of proteins, functions as a tumor suppressor in several cancers including breast cancer. However, its clinical relevance is unclear in breast cancer. In this study, expression of DLC1 was correlated with prognosis using publicly available breast cancer gene expression datasets and quantitative Reverse Transcription PCR in cohorts of Estrogen Receptor-positive (ER+) breast cancer. Mutation and methylation status of DLC1 were assessed in these datasets including The Cancer Genome Atlas (TCGA). To seek further insights in understanding the role of DLC1 in ER+ breast cancer, we developed a knock-in model of DLC1 in T47D breast cancer cells. Label-free global proteomic and TiO2 phosphopeptide enrichment assays were performed and validated using Western blotting. Here, we report that low expression of DLC1 correlates with poor prognosis in patients with ER+ breast cancer with further decrease in metastatic lesions. Analysis of the TCGA data showed that down regulation of DLC1 is not due to methylation or mutations. Stable knock-in of DLC1-full-length inhibits cell growth significantly in vitro compared to its control counterpart. 6726 phosphopeptides were quantified by phosphoproteomics analysis in both conditons, whereas 205 and 122 were unique to DLC1 knock-in and T47D-control cells, respectively. Pathway analysis using DAVID showed the top three significant clusters of differentially identified phosphopeptides involving cell-cell adhesion, mRNA processing and splicing, and transcription regulation. Decreased phosphorylation of epithelial cell transforming sequence 2 (ECT2) at the residue T359, critical for its active conformational change was validated. In conclusion, this data suggests that high expression of DLC1 reduces cell growth and is associated with favorable prognosis. Our results document an inverse relation between ECT2 phosphorylation and DLC1 expression, promising a novel strategy for treating ER+ breast cancer.

Project description:Background: CDK16 is an atypical PCTAIRE kinase, and its activity is dependent on Cyclin Y (CCNY) family. CCNYs have been reported to regulate mammary stem cell activity and mammary gland development, and CCNY plays an oncogenic role in a variety of cancers including breast cancer. However, whether CDK16 plays a role in breast cancer and whether CDK16 can be served as a therapeutic target for breast cancer remains unknown. Methods: TCGA/GEO database analysis and KM survival analysis were used to examine the mRNA expression and the clinical relevance of PFTAIRE and PCTAIRE kinases in breast cancer. The expression of CDK16 protein was determined by CPTAC dataset output and immunohistochemical analysis of breast cancer tissue microarray and immunoblot analysis of additional clinical samples. Knockdown and overexpression of CDK16 were mediated by shRNA and lentivirus vectors, respectively. Cell proliferation was assessed by colony formation and MTT analysis. The cell cycle and apoptosis were examined by FACS analysis. Wound-healing and trans-well invasion assay were conducted to test cell migration ability. The functions of CDK16 on tumorigenesis and metastasis were evaluated by cell line-derived xenograft, patient-derived organoid/xenograft, lung metastasis and systemic metastasis mouse models. RNA-sequencing analysis was performed to reveal the potential molecular mechanisms involved in the function of CDK16. Pharmacological inhibition of CDK16 was achieved by its inhibitor Rebastinib to further assess the anti-tumor effect of targeting CDK16. Results: CDK16 is highly expressed in breast cancer, especially in triple-negative breast cancer (TNBC). The elevated CDK16 expression is correlated with poor outcomes in breast cancer patients. CDK16 promotes the proliferation and migration of TNBC cells in vitro and tumorigenesis and metastasis of TNBC tumors in vivo. Both gene knockdown and pharmacological inhibition of CDK16 significantly repress tumor progression of TNBC. Mechanically, CDK16 not only regulates spindle formation by phosphorylating PRC1 at the T481 site, but also regulates the Rb-E2F pathway by phosphorylating Rb, which are essential for cell cycle progression and cell proliferation of tumor cells. Conclusion: CDK16 plays an oncogenic role in TNBC and can be served as a novel potential therapeutic target for TNBC.

Dataset Information

Pan-cancer and multi-omics analyses reveal the diagnostic and prognostic value of BAZ2B

Publications

Pan-cancer and multi-omics analyses reveal the diagnostic and prognostic value of BAZ2B in cancer.

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