Research Article
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Year 2025, Volume: 16 Issue: Erken Çevrimiçi Yayınlar
https://doi.org/10.31067/acusaglik.1557228

Abstract

References

  • 1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA Cancer J Clin. 2016 Jan-Feb;66(1):7-30. doi: 10.3322/caac.21332
  • 2. Huffman DM, Grizzle WE, Bamman MM et al.. SIRT1 is significantly elevated in mouse and human prostate cancer. Cancer Res. 2007 Jul 15;67(14):6612-8. doi: 10.1158/0008-5472.CAN-07-0085
  • 3. Bradbury CA, Khanim FL, Hayden R et al. Histone deacetylases in acute myeloid leukaemia show a distinctive pattern of expression that changes selectively in response to deacetylase inhibitors. Leukemia. 2005 Oct;19(10):1751-9. doi: 10.1038/sj.leu.2403910
  • 4. Wilking MJ, Ahmad N. The role of SIRT1 in cancer: the saga continues. Am J Pathol. 2015 Jan;185(1):26-8. doi: 10.1016/j.ajpath.2014.10.002
  • 5. Lim CS. SIRT1: tumor promoter or tumor suppressor? Med Hypotheses. 2006;67(2):341-4
  • 6. Wang RH, Sengupta K, Li C et al. Impaired DNA damage response, genome instability, and tumorigenesis in SIRT1 mutant mice. Cancer Cell. 2008 Oct 7;14(4):312-23. doi: 10.1016/j.ccr.2008.09.001
  • 7. Kuo SJ, Lin HY, Chien SY, Chen DR. SIRT1 suppresses breast cancer growth through downregulation of the Bcl-2 protein. Oncol Rep. 2013 Jul;30(1):125-30. doi: 10.3892/or.2013.2470
  • 8. microRNA Target Prediction. [Cited 2016 April 16] Available from: http://www.exiqon.com/microrna-target-prediction
  • 9. Lee J, Kemper JK. Controlling SIRT1 expression by microRNAs in health and metabolic disease. Aging (Albany NY). 2010 Aug;2(8):527-34. doi: 10.18632/aging.100184
  • 10. Lain S, Hollick JJ, Campbell J et al. Discovery, in vivo activity, and mechanism of action of a small-molecule p53 activator. Cancer Cell. 2008 May;13(5):454-63. doi: 10.1016/j.ccr.2008.03.004
  • 11. Firestein R, Blander G, Michan S et al. The SIRT1 deacetylase suppresses intestinal tumorigenesis and colon cancer growth. PLoS One. 2008 Apr 16;3(4):e2020. doi: 10.1371/journal.pone.0002020. Erratum in: PLoS One. 2024 Jun 6;19(6):e0305277. doi: 10.1371/journal.pone.0305277
  • 12. Wang RH, Zheng Y, Kim HS et al. Interplay among BRCA1, SIRT1, and Survivin during BRCA1-associated tumorigenesis. Mol Cell. 2008 Oct 10;32(1):11-20. doi: 10.1016/j.molcel.2008.09.011
  • 13. Yamakuchi M. MicroRNA Regulation of SIRT1. Front Physiol. 2012 Mar 30;3:68. doi: 10.3389/fphys.2012.00068
  • 14. Gaur A, Jewell DA, Liang Y et al. Characterization of microRNA expression levels and their biological correlates in human cancer cell lines. Cancer Res. 2007 Mar 15;67(6):2456-68. doi: 10.1158/0008-5472.CAN-06-2698
  • 15. Ito T, Yagi S, Yamakuchi M. MicroRNA-34a regulation of endothelial senescence. Biochem Biophys Res Commun. 2010 Aug 6;398(4):735-40. doi: 10.1016/j.bbrc.2010.07.012
  • 16. Fujita Y, Kojima K, Hamada N et al. Effects of miR-34a on cell growth and chemoresistance in prostate cancer PC3 cells. Biochem Biophys Res Commun. 2008 Dec 5;377(1):114-9. doi: 10.1016/j.bbrc.2008.09.086
  • 17. Kato M, Paranjape T, Müller RU et al. The mir-34 microRNA is required for the DNA damage response in vivo in C. elegans and in vitro in human breast cancer cells. Oncogene. 2009 Jun 25;28(25):2419-24. doi: 10.1038/onc.2009.106
  • 18. Nass D, Rosenwald S, Meiri E et al. MiR-92b and miR-9/9* are specifically expressed in brain primary tumors and can be used to differentiate primary from metastatic brain tumors. Brain Pathol. 2009 Jul;19(3):375-83. doi: 10.1111/j.1750-3639.2008.00184.x
  • 19. Tan HX, Wang Q, Chen LZ et al. MicroRNA-9 reduces cell invasion and E-cadherin secretion in SK-Hep-1 cell. Med Oncol. 2010 Sep;27(3):654-60. doi: 10.1007/s12032-009-9264-2
  • 20. Hildebrandt MA, Gu J, Lin J et al. Hsa-miR-9 methylation status is associated with cancer development and metastatic recurrence in patients with clear cell renal cell carcinoma. Oncogene. 2010 Oct 21;29(42):5724-8. doi: 10.1038/onc.2010.305
  • 21. Selcuklu SD, Donoghue MT, Rehmet K et al. MicroRNA-9 inhibition of cell proliferation and identification of novel miR-9 targets by transcriptome profiling in breast cancer cells. J Biol Chem. 2012 Aug 24;287(35):29516-28. doi: 10.1074/jbc.M111.335943
  • 22. Li S, Meng H, Zhou F et al. MicroRNA-132 is frequently down-regulated in ductal carcinoma in situ (DCIS) of breast and acts as a tumor suppressor by inhibiting cell proliferation. Pathol Res Pract. 2013 Mar;209(3):179-83. doi: 10.1016/j.prp.2012.12.002.
  • 23. Zhang ZG, Chen WX, Wu YH et al. MiR-132 prohibits proliferation, invasion, migration, and metastasis in breast cancer by targeting HN1. Biochem Biophys Res Commun. 2014 Nov 7;454(1):109-14. doi: 10.1016/j.bbrc.2014.10.049

Evaluation of SIRT1-Regulating miRNAs in Breast Cancer: miR-9, miR-34a, and miR-132 Expression Analysis

Year 2025, Volume: 16 Issue: Erken Çevrimiçi Yayınlar
https://doi.org/10.31067/acusaglik.1557228

Abstract

Objectives: Breast cancer is one of the most common malignancy for women and one of the most common causes of cancer related deaths for women. Genetic factors and family history play major roles in its etiology. For a possible genetic treatment genetic pathway should be illuminated.
Materials and methods: Three miRNAs known to be involved in the regulation of SIRT1 were selected for review in this study. These were miRNA-34a, miRNA-9 and miRNA-132 miRNAs. The miRNeasy Mini Kit was used to isolate total RNA from both cancer tissues and normal breast tissues in patients with breast cancer who underwent mastectomy for treatment. Expression levels of miRNAs were measured and normalized with U6 gene.
Results: After measurment of expression levels, normalizing with U6 gene and statistical analysis, we found that there was no statistically significant difference between breast cancer tissues and normal breast tissues.
Conclusion: Limited number of studies reported that the levels of all three micro RNAs were found to be lower in breast cancer tissues than in normal breast tissue. In this study, no statistically significant difference was found between normal breast tissue and breast cancer tissues in terms of levels of these micro RNAs for all three micro RNAs.
The existence of conflicting and incomplete information about the SIRT1 enzyme did not surprise us with a result that is not compatible with the literature. Further studies are needed to clearly elucidate the mechanisms of SIRT1 and its regulating micro-RNAs.
In the studies to be done, the determination of the microRNA levels simultaneously with SIRT1’s own expression levels can be enlightening on this issue.

References

  • 1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA Cancer J Clin. 2016 Jan-Feb;66(1):7-30. doi: 10.3322/caac.21332
  • 2. Huffman DM, Grizzle WE, Bamman MM et al.. SIRT1 is significantly elevated in mouse and human prostate cancer. Cancer Res. 2007 Jul 15;67(14):6612-8. doi: 10.1158/0008-5472.CAN-07-0085
  • 3. Bradbury CA, Khanim FL, Hayden R et al. Histone deacetylases in acute myeloid leukaemia show a distinctive pattern of expression that changes selectively in response to deacetylase inhibitors. Leukemia. 2005 Oct;19(10):1751-9. doi: 10.1038/sj.leu.2403910
  • 4. Wilking MJ, Ahmad N. The role of SIRT1 in cancer: the saga continues. Am J Pathol. 2015 Jan;185(1):26-8. doi: 10.1016/j.ajpath.2014.10.002
  • 5. Lim CS. SIRT1: tumor promoter or tumor suppressor? Med Hypotheses. 2006;67(2):341-4
  • 6. Wang RH, Sengupta K, Li C et al. Impaired DNA damage response, genome instability, and tumorigenesis in SIRT1 mutant mice. Cancer Cell. 2008 Oct 7;14(4):312-23. doi: 10.1016/j.ccr.2008.09.001
  • 7. Kuo SJ, Lin HY, Chien SY, Chen DR. SIRT1 suppresses breast cancer growth through downregulation of the Bcl-2 protein. Oncol Rep. 2013 Jul;30(1):125-30. doi: 10.3892/or.2013.2470
  • 8. microRNA Target Prediction. [Cited 2016 April 16] Available from: http://www.exiqon.com/microrna-target-prediction
  • 9. Lee J, Kemper JK. Controlling SIRT1 expression by microRNAs in health and metabolic disease. Aging (Albany NY). 2010 Aug;2(8):527-34. doi: 10.18632/aging.100184
  • 10. Lain S, Hollick JJ, Campbell J et al. Discovery, in vivo activity, and mechanism of action of a small-molecule p53 activator. Cancer Cell. 2008 May;13(5):454-63. doi: 10.1016/j.ccr.2008.03.004
  • 11. Firestein R, Blander G, Michan S et al. The SIRT1 deacetylase suppresses intestinal tumorigenesis and colon cancer growth. PLoS One. 2008 Apr 16;3(4):e2020. doi: 10.1371/journal.pone.0002020. Erratum in: PLoS One. 2024 Jun 6;19(6):e0305277. doi: 10.1371/journal.pone.0305277
  • 12. Wang RH, Zheng Y, Kim HS et al. Interplay among BRCA1, SIRT1, and Survivin during BRCA1-associated tumorigenesis. Mol Cell. 2008 Oct 10;32(1):11-20. doi: 10.1016/j.molcel.2008.09.011
  • 13. Yamakuchi M. MicroRNA Regulation of SIRT1. Front Physiol. 2012 Mar 30;3:68. doi: 10.3389/fphys.2012.00068
  • 14. Gaur A, Jewell DA, Liang Y et al. Characterization of microRNA expression levels and their biological correlates in human cancer cell lines. Cancer Res. 2007 Mar 15;67(6):2456-68. doi: 10.1158/0008-5472.CAN-06-2698
  • 15. Ito T, Yagi S, Yamakuchi M. MicroRNA-34a regulation of endothelial senescence. Biochem Biophys Res Commun. 2010 Aug 6;398(4):735-40. doi: 10.1016/j.bbrc.2010.07.012
  • 16. Fujita Y, Kojima K, Hamada N et al. Effects of miR-34a on cell growth and chemoresistance in prostate cancer PC3 cells. Biochem Biophys Res Commun. 2008 Dec 5;377(1):114-9. doi: 10.1016/j.bbrc.2008.09.086
  • 17. Kato M, Paranjape T, Müller RU et al. The mir-34 microRNA is required for the DNA damage response in vivo in C. elegans and in vitro in human breast cancer cells. Oncogene. 2009 Jun 25;28(25):2419-24. doi: 10.1038/onc.2009.106
  • 18. Nass D, Rosenwald S, Meiri E et al. MiR-92b and miR-9/9* are specifically expressed in brain primary tumors and can be used to differentiate primary from metastatic brain tumors. Brain Pathol. 2009 Jul;19(3):375-83. doi: 10.1111/j.1750-3639.2008.00184.x
  • 19. Tan HX, Wang Q, Chen LZ et al. MicroRNA-9 reduces cell invasion and E-cadherin secretion in SK-Hep-1 cell. Med Oncol. 2010 Sep;27(3):654-60. doi: 10.1007/s12032-009-9264-2
  • 20. Hildebrandt MA, Gu J, Lin J et al. Hsa-miR-9 methylation status is associated with cancer development and metastatic recurrence in patients with clear cell renal cell carcinoma. Oncogene. 2010 Oct 21;29(42):5724-8. doi: 10.1038/onc.2010.305
  • 21. Selcuklu SD, Donoghue MT, Rehmet K et al. MicroRNA-9 inhibition of cell proliferation and identification of novel miR-9 targets by transcriptome profiling in breast cancer cells. J Biol Chem. 2012 Aug 24;287(35):29516-28. doi: 10.1074/jbc.M111.335943
  • 22. Li S, Meng H, Zhou F et al. MicroRNA-132 is frequently down-regulated in ductal carcinoma in situ (DCIS) of breast and acts as a tumor suppressor by inhibiting cell proliferation. Pathol Res Pract. 2013 Mar;209(3):179-83. doi: 10.1016/j.prp.2012.12.002.
  • 23. Zhang ZG, Chen WX, Wu YH et al. MiR-132 prohibits proliferation, invasion, migration, and metastasis in breast cancer by targeting HN1. Biochem Biophys Res Commun. 2014 Nov 7;454(1):109-14. doi: 10.1016/j.bbrc.2014.10.049
There are 23 citations in total.

Details

Primary Language English
Subjects Surgery (Other)
Journal Section Research Articles
Authors

Muhsin Elçi 0000-0003-1926-9248

Alper Aytekin 0000-0003-2872-5276

Nurullah Aksoy 0000-0002-6284-0684

Göktürk Maralcan 0000-0002-5057-7102

Early Pub Date March 21, 2025
Publication Date
Submission Date September 27, 2024
Acceptance Date January 28, 2025
Published in Issue Year 2025Volume: 16 Issue: Erken Çevrimiçi Yayınlar

Cite

EndNote Elçi M, Aytekin A, Aksoy N, Maralcan G (March 1, 2025) Evaluation of SIRT1-Regulating miRNAs in Breast Cancer: miR-9, miR-34a, and miR-132 Expression Analysis. Acıbadem Üniversitesi Sağlık Bilimleri Dergisi 16 Erken Çevrimiçi Yayınlar