Related Experiment Video

Updated: Jun 24, 2026

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
11:13

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration

Published on: June 9, 2023

miR-145 inhibits breast cancer cell growth through RTKN

Shihua Wang1, Chunjing Bian, Zhuo Yang

  • 1Center of Tissue Engineering, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, P.R. China.

International Journal of Oncology
|April 11, 2009
PubMed

Insights

MicroRNA-145 (miR-145) is downregulated in breast cancer cells, inhibiting growth and inducing apoptosis. Its targeting of RTKN suggests a mechanism for cancer cell proliferation.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression.
  • Aberrant miRNA expression is linked to various human cancers.
  • Understanding miRNA roles is crucial for cancer research.

Purpose of the Study:

  • To investigate the role of miR-145 in breast cancer.
  • To identify potential targets of miR-145 in cancer cells.
  • To elucidate the mechanism by which miR-145 affects cancer cell growth.

Main Methods:

  • Comparison of miR-145 expression in breast cancer cell lines (MCF-7) and normal cells (MCF10A).
  • Overexpression of miR-145 using plasmid vectors.
  • Bioinformatic analysis to predict miR-145 targets.
  • Reporter assays to confirm direct binding of miR-145 to the RTKN 3'UTR.
  • siRNA-mediated knockdown of RTKN.

Main Results:

  • miR-145 was significantly downregulated in MCF-7 cells compared to MCF10A cells.
  • Overexpression of miR-145 inhibited MCF-7 cell proliferation and induced apoptosis.
  • RTKN was identified as a direct target of miR-145.
  • miR-145 overexpression reduced both mRNA and protein levels of RTKN.
  • siRNA-mediated knockdown of RTKN also inhibited MCF-7 cell growth.

Conclusions:

  • Loss of miR-145 contributes to breast cancer cell growth by upregulating RTKN.
  • miR-145 acts as a tumor suppressor in breast cancer by targeting RTKN.
  • Targeting the miR-145/RTKN axis may offer a therapeutic strategy for breast cancer.

More Related Videos

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...
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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
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 rapamycin-insensitive companion...