CtBP modulates Snail-mediated tumor invasion in Drosophila

Cell Death Discovery, 2021 · DOI: https://doi.org/10.1038/s41420-021-00516-x · Published: May 14, 2021

Simple Explanation

Cancer is a dangerous disease, and metastasis is a major reason why it's so deadly. The protein CtBP is found in high levels in many cancers, making it a target for new treatments. This study found that CtBP, along with another protein called Snail, promotes tumor growth and spread in fruit flies. They showed that these proteins are needed for tumor cells to move and invade other tissues. The study suggests that CtBP and Snail work together to activate a signaling pathway (JNK) that is important for tumor invasion. Blocking these proteins could be a new way to treat cancer.

Study Duration

Not specified

Participants

Drosophila melanogaster

Evidence Level

In vivo experimental study

Key Findings

1
Depletion of CtBP or Snail (Sna) suppressed RasV12/lgl-/--triggered tumor growth and invasion, and disrupted cell polarity-induced invasive cell migration in Drosophila.
2
Loss of CtBP inhibits RasV12/Sna-induced tumor invasion and Sna-mediated invasive cell migration.
3
CtBP is essential for Sna-mediated EMT processes, although ectopic expression of CtBP alone did not produce any EMT-like phenotype.

Research Summary

This study investigates the role of CtBP and Snail in tumor invasion using Drosophila as a model organism. The researchers found that both CtBP and Snail are required for tumor growth and invasion triggered by specific genetic mutations. The study demonstrates that CtBP is essential for Snail-mediated tumor invasion and EMT. CtBP and Sna regulate cell migration in thorax development. The findings suggest that CtBP interacts with Snail to form a transcriptional complex that activates the JNK signaling pathway, promoting cell migration and tumor invasion. This provides insights for potential therapeutic strategies for cancer treatment.

Practical Implications

Therapeutic Target Identification

CtBP and Snail may be potential therapeutic targets for cancer treatment, particularly in preventing tumor metastasis.

Drug Development

The interaction between CtBP and Snail, and their involvement in the JNK signaling pathway, suggests opportunities for developing drugs that disrupt this interaction or inhibit the pathway.

Clinical Strategies

Understanding the role of CtBP and Snail in EMT could lead to clinical strategies aimed at preventing or reversing EMT in cancer patients.

Study Limitations

1
The study was conducted in Drosophila, which may not fully represent the complexity of human cancers.
2
Further research is needed to verify the contribution of CtBP and JNK in Snail-induced EMT in human cancers.
3
The exact molecular mechanisms of how CtBP and Snail interact to regulate the JNK signaling pathway still require further elucidation.

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