Investigating the Molecular Mechanisms and Therapeutic Implications of Soybean Consumption in Breast Cancer
Abstract
Background: Breast cancer is the leading cause of cancer mortality in women. Studies indicate that soybeans contain powerful compounds that may play a beneficial role in preventing and treating breast cancer. Objective: This study aims to identify differentially expressed genes (DEGs) and pathways associated with soy consumption in breast cancer patients. Methods: Four microarray datasets were analyzed using GEO2R to identify DEGs (|logFC| > 1, p < 0.05). Venn diagrams identified common genes across studies. Breast cancer-specific genes were further isolated from the DEGs using the GEPIA database, with a focus on candidate genes and signaling pathways influenced by soybean consumption and its therapeutic effects on breast cancer. Results: The analysis revealed that soy consumption correlated with the upregulation of pathways like cell senescence, actin cytoskeleton regulation, and apoptosis processes often heightened in breast cancer. Conversely, pathways such as the cell cycle and p53 signaling were downregulated. Notably, the cell cycle pathway, pivotal in breast cancer, exhibited downregulation of key genes (CDC20, CCNB1, CDC6, MAD2L1, CCNA2, TTK, MCM4, CDC25C, MCM2, and ESPL1), which are critical for cell cycle progression and checkpoint regulation. Dysregulation of these genes is associated with cancer development. Additionally, soy and its derivatives may activate pathways like PI3K/Akt signaling and epithelial-mesenchymal transition. Conclusion: The results indicate that soy-derived compounds could offer a promising therapeutic approach for breast cancer by altering gene expression patterns linked to the disease.
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References
Qiu S, Jiang CJEjon(s). Soy and isoflavones consumption and breast cancer survival and recurrence: a systematic review and meta-analysis. 2019;58(8):3079-90. doi: 10.1007/s00394-018-1853-4.
Harbeck N, Penault-Llorca F, Cortes J, Gnant M, Houssami N, Poortmans P, et al. Breast cancer Nat Rev Dis Primers 5: 66. ed; 2019.
McLay JS, Stewart D, George J, Rore C, Heys SDJEjocp(s). Complementary and alternative medicines use by Scottish women with breast cancer. What, why and the potential for drug interactions? 2012;68(5):811-9. doi: 10.1007/s00228-011-1181-6.
Dong J-Y, Qin L-QJBcr, treatment(s). Soy isoflavones consumption and risk of breast cancer incidence or recurrence: a meta-analysis of prospective studies. 2011;125(2):315-23. doi: 10.1007/s10549-010-1270-8.
GolKhoo S, Ahmadi A, Hanachi P, Barantalab F, Vaziri MJPJoBS(s). Determination of daidzein and genistein in soy milk in Iran by using HPLC analysis method. 2008;11(18):2254-8. doi: 10.3923/pjbs.2008.2254.2258.
Shike M, Doane AS, Russo L, Cabal R, Reis-Filho JS, Gerald W, et al.(s). The effects of soy supplementation on gene expression in breast cancer: a randomized placebo-controlled study. 2014;106(9):doi: 10.1093/jnci/dju189.
Lie Yuan YC, Liang Zhang, Sijia Liu , Pan Li, Xiaoli Li(s). Promoting Apoptosis, a Promising Way to Treat Breast Cancer With Natural Products: A Comprehensive Review. Front Pharmacology. 2022;28(12:80166):doi: 10.3389/fphar.2021.801662.
Rietjens IM, Sotoca AM, Vervoort J, Louisse JJMn, research f(s). Mechanisms underlying the dualistic mode of action of major soy isoflavones in relation to cell proliferation and cancer risks. 2013;57(1):100-13. doi: 10.1002/mnfr.201200439.
Lawrence MS, Stojanov P, Mermel CH, Robinson JT, Garraway LA, Golub TR, et al.(s). Discovery and saturation analysis of cancer genes across 21 tumour types. 2014;505(7484):495-501. doi: 10.1038/nature12912.
Shao C, Huang Y, Fu B, Pan S, Zhao X, Zhang N, et al.(s). Targeting c-Jun in A549 cancer cells exhibits antiangiogenic activity in vitro and in vivo through exosome/miRNA-494-3p/PTEN signal pathway. 2021;11(663183. doi: 10.3389/fonc.2021.663183.
Lukey MJ, Greene KS, Erickson JW, Wilson KF, Cerione RAJNC(s). The oncogenic transcription factor c-Jun regulates glutaminase expression and sensitizes cells to glutaminase-targeted therapy. 2016;7(1):11321. doi: 10.1038/ncomms11321.
Thu K, Soria-Bretones I, Mak T, Cescon DJCC(s). Targeting the cell cycle in breast cancer: towards the next phase. 2018;17(15):1871-85. doi: 10.1080/15384101.2018.1502567.
Cappello P, Blaser H, Gorrini C, Lin D, Elia A, Wakeham A, et al.(s). Role of Nek2 on centrosome duplication and aneuploidy in breast cancer cells. 2014;33(18):2375-84. doi: 10.1038/onc.2013.183.
Hao Z, Zhang H, Cowell JJTB(s). Ubiquitin-conjugating enzyme UBE2C: molecular biology, role in tumorigenesis, and potential as a biomarker. 2012;33(3):723-30. doi: 10.1007/s13277-011-0291-1.
Chou C-P, Huang N-C, Jhuang S-J, Pan H-B, Peng N-J, Cheng J-T, et al.(s). Ubiquitin-conjugating enzyme UBE2C is highly expressed in breast microcalcification lesions. 2014;9(4):e93934. doi: 10.1371/journal.pone.0093934.
Lin F, Xie Y-J, Zhang X-K, Huang T-J, Xu H-F, Mei Y, et al.(s). GTSE1 is involved in breast cancer progression in p53 mutation-dependent manner. 2019;38(1):152. doi: 10.1186/s13046-019-1157-4.
Zeng C-M, Chang L-L, Ying M-D, Cao J, He Q-J, Zhu H, et al.(s). Aldo–keto reductase AKR1C1–AKR1C4: Functions, regulation, and intervention for anti-cancer therapy. 2017;8(119. doi: 10.3389/fphar.2017.00119.
Shin VY, Chen J, Cheuk IW-Y, Siu M-T, Ho C-W, Wang X, et al.(s). Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness. 2019;10(4):270. doi: 10.1038/s41419-019-1513-5.
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