Related Experiment Video

Updated: Jan 4, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

8.0K

MicroRNA‑125a‑5p controls the proliferation, apoptosis, migration and PTEN/MEK1/2/ERK1/2 signaling pathway in MCF‑7

Zhongzeng Liang1, Qunwen Pan2, Zhi Zhang1

  • 1Department of Vascular Thyroid Breast Surgery, Institute of Neurology, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, P.R. China.

Molecular Medicine Reports
|November 9, 2019
PubMed

Insights

MicroRNA-125a-5p suppresses breast cancer cell proliferation and migration while promoting apoptosis. This microRNA targets PTEN, MEK/ERK signaling, and apoptosis-related proteins, suggesting its potential in breast cancer gene therapy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • MicroRNA (miR)-125a-5p shows tumor-suppressive potential, but its role in breast cancer remains unclear.
  • Understanding miR-125a-5p's function in breast cancer is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the effects of miR-125a-5p on MCF-7 breast cancer cells.
  • To elucidate the underlying molecular mechanisms of miR-125a-5p action in breast cancer.

Main Methods:

  • MCF-7 cells were manipulated for miR-125a-5p overexpression or knockdown.
  • Cell proliferation, migration, and apoptosis were assessed using MTT, scratch, and flow cytometry assays.
  • Protein and gene expression levels of PTEN, MEK/ERK pathway components, Bcl-2, and caspase-3 were analyzed via Western blotting and RT-qPCR.

Main Results:

  • miR-125a-5p overexpression inhibited MCF-7 cell proliferation and migration.
  • Apoptosis was significantly increased in miR-125a-5p overexpressing cells.
  • These changes correlated with increased PTEN and cleaved caspase-3, and decreased p-MEK1/2, p-ERK1/2, and Bcl-2 expression.

Conclusions:

  • miR-125a-5p regulates breast cancer cell functions by modulating PTEN, MEK/ERK signaling, and apoptosis pathways.
  • miR-125a-5p demonstrates potential as a therapeutic target for breast cancer gene therapy.

More Related Videos

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells09:45

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

8.8K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.2K

Related Concept Videos

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...
4.6K
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...
3.7K
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...
23.8K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.2K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.8K
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...
5.0K