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Related Experiment Video

Updated: May 14, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

A splicing twist on metastasis.

Oakley C Olson¹, Johanna A Joyce

¹Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

Science Translational Medicine

|January 25, 2013

Summary

This summary is machine-generated.

A KLF6 splice variant drives breast cancer metastasis and poor survival by promoting epithelial-to-mesenchymal transition. This oncogenic factor regulates the Twist pathway, highlighting a potential therapeutic target for aggressive breast cancer.

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Area of Science:

Oncology
Molecular Biology
Cancer Genetics

Background:

The transcription factor KLF6 plays a role in cell growth and differentiation.
Aberrant KLF6 splicing can lead to oncogenic variants with implications in cancer progression.

Purpose of the Study:

To investigate the role of an oncogenic splice variant of KLF6 in breast cancer.
To determine the association of this variant with patient survival and metastasis.
To elucidate the molecular mechanisms by which this variant promotes cancer progression, specifically epithelial-to-mesenchymal transition (EMT).

Main Methods:

Analysis of KLF6 splice variants in breast cancer patient samples.
Correlation studies between variant presence and clinical outcomes (metastasis, survival).
In vitro experiments to assess the impact of the KLF6 variant on EMT markers and the regulation of Twist.

Main Results:

An oncogenic splice variant of KLF6 was identified and associated with poor survival in node-negative breast cancer patients.
This KLF6 variant significantly promotes the epithelial-to-mesenchymal transition (EMT).
The oncogenic KLF6 variant was found to regulate the expression or activity of Twist, a key EMT regulator.

Conclusions:

The oncogenic KLF6 splice variant is a marker of poor prognosis in node-negative breast cancer.
KLF6 splice variants contribute to breast cancer aggressiveness by driving EMT through Twist regulation.
Targeting this specific KLF6 variant or its downstream pathways may offer new therapeutic strategies for metastatic breast cancer.