Version 1
: Received: 7 December 2023 / Approved: 8 December 2023 / Online: 8 December 2023 (13:11:58 CET)
How to cite:
Anyomi, B.K.; Fosu, K.; Kampo, S.; Liu, T.; Wei, J. In-Silico Molecular Analysis of the Inverse Interaction between Cancer and Alzheimer’s Disease. Preprints2023, 2023120603. https://doi.org/10.20944/preprints202312.0603.v1
Anyomi, B.K.; Fosu, K.; Kampo, S.; Liu, T.; Wei, J. In-Silico Molecular Analysis of the Inverse Interaction between Cancer and Alzheimer’s Disease. Preprints 2023, 2023120603. https://doi.org/10.20944/preprints202312.0603.v1
Anyomi, B.K.; Fosu, K.; Kampo, S.; Liu, T.; Wei, J. In-Silico Molecular Analysis of the Inverse Interaction between Cancer and Alzheimer’s Disease. Preprints2023, 2023120603. https://doi.org/10.20944/preprints202312.0603.v1
APA Style
Anyomi, B.K., Fosu, K., Kampo, S., Liu, T., & Wei, J. (2023). In-Silico Molecular Analysis of the Inverse Interaction between Cancer and Alzheimer’s Disease. Preprints. https://doi.org/10.20944/preprints202312.0603.v1
Chicago/Turabian Style
Anyomi, B.K., Tingting Liu and Jianshe Wei. 2023 "In-Silico Molecular Analysis of the Inverse Interaction between Cancer and Alzheimer’s Disease" Preprints. https://doi.org/10.20944/preprints202312.0603.v1
Abstract
Introduction: Depending on the kind of cancer and neurological disorders, there might be a direct or inverse link between neurodegeneration and cancer. The inverse interaction between cancer and Alzheimer's pathology has garnered substantial interest in medical research. While this inverse interaction between Alzheimer's pathology and cancer presents a fascinating scientific puzzle, there is still limited information and studies on the potential mechanisms involved in this inverse rela-tionship. Aim: This study aims to identify potential genes from Alzheimer's disease that may protect against cancer.
Method: The Gene Expression Omnibus (GEO) database provided the Alzheimer's pathology dataset, and GEO 2R was utilized to examine genes that were differentially expressed. The expression of upregulated Alzheimer's pathology genes in breast, colorectal, and prostate cancer was compared using VENN 2.1, colorectal, and prostate cancer was compared using VENN 2.1, and colorectal and prostate cancers were compared using VENN 2.1.
Results: Among the upregulated genes associated with Alzheimer's disease, 25 genes are shared among breast cancer, colorectal cancer, and prostate cancer, while 28 of these genes were exclusive to Alzheimer's dis-ease. Gene expression profiling interactive analysis among the shared genes revealed that AQP1, C4A, CSRP2, CRYAB, MACF1, HSPB2, and NEAT1 were downregulated in breast, colorectal, and prostate cancers. These genes have varying roles in cancer progression and suppression. Functional analysis of Alzheimer's disease-related upregulated genes revealed that C1orf56 and HIST1H2AC control cell proliferation, with HIST1H2AC playing a role in necroptosis. Additionally, C1orf56 worked as an oncogenic modifier to support DNMT3B's tumor suppressor properties.
Conclusion: Given the role of HIST1H2AC and C1orf56 in the negative control of cell proliferation and their upregulation in Alzheimer's disease, there is a need to further investigate HIST1H2AC and C1orf56 as potential tumor suppressors responsible for Alzheimer's disease and cancer inverse association.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
