Genistein-induced mir-23b expression inhibits the growth of breast cancer cells

Related Experiment Video

Updated: Apr 6, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
08:40

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Published on: April 6, 2012

18.1K

Cigir Biray Avci1, Sunde Yilmaz Susluer1, Hasan Onur Caglar2

  • 1Department of Medical Biology, Medical Faculty, Ege University, Bornova, Izmir, Turkey.

Contemporary Oncology (Poznan, Poland)
|July 23, 2015
PubMed
Abstract

Insights

Genistein treatment significantly up-regulated miR-23b expression in MCF-7 breast cancer cells. This microRNA may serve as a potential biomarker for genistein therapy response in breast cancer.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Genistein, an isoflavonoid, exhibits anti-cancer properties by inhibiting protein tyrosine kinase phosphorylation, inducing apoptosis, and promoting cell differentiation.
  • Breast cancer treatment strategies often involve targeting specific molecular pathways and cellular processes.

Purpose of the Study:

  • To investigate the impact of genistein-induced cellular stress on miRNA expression profiles in MCF-7 breast cancer cells.
  • To identify specific microRNAs (miRNAs) whose expression is altered by genistein treatment.

Main Methods:

  • Cytotoxicity of genistein was assessed using XTT and trypan blue dye exclusion assays.
  • MiRNA expression levels were quantified using Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction (RT-qPCR).

Main Results:

  • The half-maximal inhibitory concentration (IC50) of genistein in MCF-7 cells was determined to be 175 μM.
  • Genistein treatment for 48 hours induced a significant cytotoxic effect.
  • A notable 56.69-fold upregulation of miR-23b was observed in MCF-7 cells following genistein exposure.

Conclusions:

  • Upregulated expression of miR-23b may indicate a potential biomarker for genistein therapy in breast cancer patients.
  • The observed miR-23b upregulation could be crucial for predicting response to genistein treatment.
Keywords:
MCF-7breast cancergenisteinmiRNA

More Related Videos

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells16:24

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells

Published on: February 21, 2014

20.8K
Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization06:01

Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization

Published on: June 7, 2016

7.2K

Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
24.7K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
4.3K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.4K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.1K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.3K