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Integrated Pan-Cancer Profiling and Breast Cancer Validation Identify BEND3 as a Potential Prognostic and Immune
Yuting Gou1, Yongxiang Li1, Yiyang Wang1
1Department of Breast Surgery, Center of Digestive and Vascular, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, People's Republic of China.
Purpose:
BEND3 is implicated in various physiological processes, including chromatin regulation, cell cycle regulation, etc.; nonetheless, its function in cancer is not well comprehended.
Methods:
Using public databases including UCSC Xena, TCGA, GTEx, and GEO, we conducted a comprehensive pan-cancer analysis to evaluate the clinical relevance of BEND3 across 33 cancer types. We analyzed genetic alterations, copy number variations (CNVs), and methylation profiles of BEND3, and explored its associations with tumor mutational burden (TMB), microsatellite instability (MSI), immune checkpoint molecules, and the tumor immune microenvironment. A protein-protein interaction (PPI) network and functional enrichment analysis were performed to investigate potential molecular mechanisms. In vitro, BEND3 expression was assessed by immunohistochemistry (IHC), Western blot (WB), and qRT-PCR. Cell Counting Kit-8 (CCK-8), colony formation, and wound healing assays were performed to validate BEND3's oncogenic role in breast cancer cell lines.
Results:
Our results show that BEND3 is frequently overexpressed in multiple cancers, including breast, liver, lung, thyroid, and gastric cancers, among others, and is associated with poor prognosis. Its expression correlates with TMB, MSI, immune checkpoint molecules, and immunoinfiltration, suggesting a role in tumor immunity. Functional analysis indicates involvement in key cancer-related pathways. In breast cancer, BEND3 was upregulated in clinical tissues and cell lines, and in vitro experiments demonstrated that BEND3 overexpression promoted the proliferation, migration, and invasion of breast cancer cells, whereas its knockdown suppressed these phenotypes.
Conclusion:
Our findings suggest BEND3 is a potential prognostic and immune-related cancer biomarker. Its overexpression in multiple cancers, association with poor survival, and role in tumor immunity support its oncogenic function. Functional analysis indicates it may regulate key cancer pathways. Importantly, in vitro experiments confirm its tumor-promoting effects in breast cancer, providing a foundation for further study of BEND3's mechanisms and therapeutic implications.
Insights
The study reveals that BEND3 is overexpressed in many cancers and linked to poor prognosis. BEND3 promotes cancer cell proliferation and invasion, suggesting its potential as a prognostic biomarker.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The function of BEND3 in cancer remains poorly understood despite its known roles in chromatin and cell cycle regulation.
- Understanding BEND3's role is crucial for identifying new cancer biomarkers and therapeutic targets.
Purpose of the Study:
- To conduct a comprehensive pan-cancer analysis of BEND3's clinical relevance and explore its molecular mechanisms in cancer.
- To investigate the oncogenic role of BEND3 in breast cancer cell lines.
Main Methods:
- Utilized public databases (UCSC Xena, TCGA, GTEx, GEO) for pan-cancer analysis of BEND3 genetic alterations, CNVs, and methylation.
- Assessed BEND3 expression via IHC, WB, and qRT-PCR; evaluated its role in proliferation, migration, and invasion using CCK-8, colony formation, and wound healing assays in breast cancer cells.
Main Results:
- BEND3 is frequently overexpressed in multiple cancers (e.g., breast, liver, lung) and associated with poor prognosis.
- BEND3 expression correlates with tumor mutational burden, microsatellite instability, immune checkpoints, and immune infiltration.
- In vitro studies confirmed BEND3 overexpression promotes breast cancer cell proliferation, migration, and invasion, while knockdown suppresses these phenotypes.
Conclusions:
- BEND3 is a potential prognostic and immune-related biomarker in cancer due to its overexpression, association with poor survival, and role in tumor immunity.
- BEND3 exhibits oncogenic functions and may regulate key cancer pathways, warranting further investigation into its mechanisms and therapeutic potential.
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