Research Article

Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells

Volume: 20 Number: 3 September 30, 2024
EN

Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells

Abstract

Micro RNAs (miRNA) play a role in basic cellular processes such as cell growth, development, cell cycle and apoptosis by affecting gene expression. Abnormal regulation or changes in expression of miRNAs can be observed in many diseases, especially cancer. Therefore, miRNAs are also being investigated as potential therapeutic targets. It has been suggested that miR-506 may be expressed at low levels in various types of cancer and this may contribute to cancer development. In this study, the effect of miR-506 on the sensitivity of breast cancer cells to metformin was evaluated in terms of its effect on cell survival and apoptotic mechanism. Metformin caused a dose-dependent decrease in cell viability and induced loss of mitochondrial membrane potential in MCF-7 cells while MDA-MB-231 cells were more resistant. The colony formation and migration potential of both cell lines with increased miR-506 expression were significantly suppressed after metformin treatment. Additionally, apoptotic cell death triggered by metformin was induced in both cell lines when miR-506 expression was increased. In conclusion, miR-506 acts as a tumor suppressor in MCF-7 and MDA-MB-231 cells and increases their sensitivity to metformin, indicating the potential of miR-506 to be an important therapeutic target in future studies.

Keywords

Supporting Institution

İstanbul Kültür Üniversitesi

Ethical Statement

There are no ethical issues after the publication of this manuscript.

Thanks

The authors wish to thank Scientific Research Projects Unit of Istanbul Kultur University for their constant interest in this project.

References

  1. [1]. Otmani K., Lewalle P. 2021. Tumor Suppressor miRNA in Cancer Cells and the Tumor Microenvironment: Mechanism of Deregulation and Clinical Implications. Front. Oncol.; 11: 708-765.
  2. [2]. Michlewski G., Cáceres J. F. 2019. Post-transcriptional control of miRNA biogenesis. RNA; 25(1): 1–16.
  3. [3]. Muñoz J. P., Pérez-Moreno P., Pérez Y., Calaf G. M. 2023. The Role of MicroRNAs in Breast Cancer and the Challenges of Their Clinical Application., Diagnostics (Basel, Switzerland); 13(19): 3072.
  4. [4]. Annese T., Tamma R., De Giorgis M., Ribatti D. 2020. microRNAs Biogenesis, Functions and Role in Tumor Angiogenesis., Front. Oncol.; 10(1): 581007-58127.
  5. [5]. Wen S.Y., Lin Y., Yu YQ., Cao S.J., Zhang R., Yang X.M., Li J., Zhang Y.L., Wang Y.H., Ma M.Z., Sun W.W., Lou X.L., Wang J.H., Teng Y.C., Zhang Z.G. 2015. miR-506 acts as a tumor suppressor by directly targeting the hedgehog pathway transcription factor Gli3 in human cervical cancer. Oncogene; 34(6): 717–725.
  6. [6]. Saad El Din G., Youness R. A., Assal R. A., Gad M. Z. 2018. Mir-506-3p synergistically represses breast cancer progression through altering cell cycle regulators. Ann. Oncol; 29: 28-34.
  7. [7]. Lu C.C., Chiang J.H., Tsai F.J., Hsu Y.M., Juan Y.N., Yang J.S., Chiu H.Y. 2019. Metformin triggers the intrinsic apoptotic response in human AGS gastric adenocarcinoma cells by activating AMPK and suppressing mTOR/AKT signaling, Metformin triggers the intrinsic apoptotic response in human AGS gastric adenocarcinoma cells by activating AMPK and suppressing mTOR/AKT signaling. Int. J. Oncol; 54(4): 1271–1281.
  8. [8]. Balkan B., Demir G., Balkan F., Çetingök H., Atiç E. 2020. Metformin İlişkili Laktik Asidoz; Bir Olgu Nedeni ile Literatürün Gözden Geçirilmesi, Tıp Fakültesi Klinikleri Dergisi; 3(1): 49-53.

Details

Primary Language

English

Subjects

Nanochemistry

Journal Section

Research Article

Publication Date

September 30, 2024

Submission Date

March 15, 2024

Acceptance Date

July 6, 2024

Published in Issue

Year 2024 Volume: 20 Number: 3

APA
Rencuzoğulları, Ö., & Qayoumi, S. (2024). Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells. Celal Bayar University Journal of Science, 20(3), 1-9. https://doi.org/10.18466/cbayarfbe.1453535
AMA
1.Rencuzoğulları Ö, Qayoumi S. Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells. CBUJOS. 2024;20(3):1-9. doi:10.18466/cbayarfbe.1453535
Chicago
Rencuzoğulları, Özge, and Suraya Qayoumi. 2024. “Investigation the Role of MiR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells”. Celal Bayar University Journal of Science 20 (3): 1-9. https://doi.org/10.18466/cbayarfbe.1453535.
EndNote
Rencuzoğulları Ö, Qayoumi S (September 1, 2024) Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells. Celal Bayar University Journal of Science 20 3 1–9.
IEEE
[1]Ö. Rencuzoğulları and S. Qayoumi, “Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells”, CBUJOS, vol. 20, no. 3, pp. 1–9, Sept. 2024, doi: 10.18466/cbayarfbe.1453535.
ISNAD
Rencuzoğulları, Özge - Qayoumi, Suraya. “Investigation the Role of MiR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells”. Celal Bayar University Journal of Science 20/3 (September 1, 2024): 1-9. https://doi.org/10.18466/cbayarfbe.1453535.
JAMA
1.Rencuzoğulları Ö, Qayoumi S. Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells. CBUJOS. 2024;20:1–9.
MLA
Rencuzoğulları, Özge, and Suraya Qayoumi. “Investigation the Role of MiR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells”. Celal Bayar University Journal of Science, vol. 20, no. 3, Sept. 2024, pp. 1-9, doi:10.18466/cbayarfbe.1453535.
Vancouver
1.Özge Rencuzoğulları, Suraya Qayoumi. Investigation the Role of miR-506 in Metformin-Induced Cell Death Mechanism in MCF-7 and MDA-MB-231 Breast Cancer Cells. CBUJOS. 2024 Sep. 1;20(3):1-9. doi:10.18466/cbayarfbe.1453535