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Updated: Oct 21, 2025

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
CG7379 and ING1 suppress cancer cell invasion by maintaining cell-cell junction integrity
Alexandra D Rusu1,2, Zoe E Cornhill1, Brenda Canales Coutiño1,3
1School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK.
Abstract:
Approximately 90% of cancer-related deaths can be attributed to a tumour's ability to spread. We have identified CG7379, the fly orthologue of human ING1, as a potent invasion suppressor. ING1 is a type II tumour suppressor with well-established roles in the transcriptional regulation of genes that control cell proliferation, response to DNA damage, oncogene-induced senescence and apoptosis. Recent work suggests a possible role for ING1 in cancer cell invasion and metastasis, but the molecular mechanism underlying this observation is lacking. Our results show that reduced expression of CG7379 promotes invasion in vivo in Drosophila, reduces the junctional localization of several adherens and septate junction components, and severely disrupts cell-cell junction architecture. Similarly, ING1 knockdown significantly enhances invasion in vitro and disrupts E-cadherin distribution at cell-cell junctions. A transcriptome analysis reveals that loss of ING1 affects the expression of several junctional and cytoskeletal modulators, confirming ING1 as an invasion suppressor and a key regulator of cell-cell junction integrity.
Insights
The fly gene CG7379, similar to human ING1, suppresses cancer cell invasion. Loss of this gene disrupts cell-cell junctions, promoting tumor spread.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Tumor metastasis is a major cause of cancer mortality.
- The ING1 gene is a known tumor suppressor involved in DNA damage response and cell cycle control.
- The precise role of ING1 in cancer cell invasion and metastasis remains unclear.
Purpose of the Study:
- To investigate the role of CG7379, the fly orthologue of human ING1, as a potential suppressor of cancer cell invasion.
- To elucidate the molecular mechanisms by which ING1 influences cell-cell junction integrity and tumor metastasis.
Main Methods:
- Utilized *Drosophila* *in vivo* models to study CG7379 function.
- Performed *in vitro* experiments with ING1 knockdown in mammalian cells.
- Analyzed cell-cell junction architecture and component localization.
- Conducted transcriptome analysis to identify affected genes.
Main Results:
- Reduced CG7379 expression in *Drosophila* promoted tumor invasion and disrupted adherens and septate junctions.
- ING1 knockdown in mammalian cells enhanced invasion and disrupted E-cadherin localization at cell-cell junctions.
- Loss of ING1 altered the expression of genes regulating cell junctions and the cytoskeleton.
Conclusions:
- CG7379/ING1 acts as a potent suppressor of cancer cell invasion.
- ING1 is crucial for maintaining cell-cell junction integrity.
- ING1 regulates invasion through modulation of junctional and cytoskeletal components.
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