Unveiling the potential role of ARID3A in the colon adenocarcinoma Immune Microenvironment using TCGA Data

Author:

Baldi Salem1,Gao Yaqin2,Mohammed Shadi A.D.3,Alnadari Fawze4,AL-Mogahed Maged5,Alazizi Esmail M. Y.6

Affiliation:

1. Department of Medical Laboratory, Al-Thawra General Hospital, Hodeidah, Yemen

2. Department of ultrasound diagnosis, Zhongda Hospital Southeast University, Nanjing, 210009, China

3. Department of Pharmacy, Faculty of Medical Sciences, Al Janad University for Science and Technology, Taiz, Yemen

4. Research and Development Center of Jiangsu Tianmeijian Nature Bioengineering Co., Ltd., China

5. Department of Surgery, The First Bethune Hospital of Jilin University, Changchun, Jilin province, 130012 China

6. Sichuan University of Science and Engineering, Zigong, Sichuan, 643000, China

Abstract

Abstract The tumour microenvironment can be shaped by tumour-infiltrating immune cells that control the fate of immunotherapy effects. The association between AT-rich interactive domain-containing protein 3A (ARID3A) and immune cell infiltration and oxidative stress in colon adenocarcinoma (COAD) remains unknown. In the current study, we explored the correlation between ARID3A expression, immune cell infiltration, and potential pathological pathways in COAD. ARID3A expression level in COAD were analyzed by the TNMplot and GEPIA2 using COAD TCGA databases. ARID3A expression was significantly higher in COAD tissues than adjacent normal tissues and associated with adverse outcome in COAD patients. Immunohistochemistry staining for ARID3A reveals no positivity staining in normal human colon tissue but varying degrees of positivity in malignant colon tissue. ARID3A showed a strong negative correlation with tumour-infiltrating NK and CD8+ T cells, and a positive correlation with macrophages and neutrophils infiltration in COAD patients. These findings suggest that ARID3A is a potential prognostic biomarker that could promote COAD progression and negatively correlates with tumor immune cells infiltration in the COAD microenvironment. ARID3A gene affects cellular oxidative stress and other important pathological pathways in cancer. In conclusion, ARID3A may improve tumor cell survival by activating the PI3K-AKT-mTOR pathway, which accelerates ECM breakdown, facilitates invasion, suppresses apoptosis, and prevents cell death. This study might contribute to uncovering the mechanism and providing a new strategy of diagnosis and therapies for COAD. Further studies are warranted on current topic.

Publisher

Research Square Platform LLC

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