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MUC1-C drives MYC in multiple myeloma
Ashujit Tagde1, Hasan Rajabi1, Audrey Bouillez1
1Department of Medical Oncology, Dana-Farber Cancer Institute.
Blood
|February 25, 2016
Summary
Multiple myeloma cells rely on the MYC oncoprotein. Targeting the MUC1-C protein reduces MYC expression and its downstream genes, revealing a new therapeutic strategy for multiple myeloma.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Multiple myeloma (MM) cells depend on the MYC oncoprotein for survival.
- The mechanisms driving MYC upregulation in MM remain largely unknown.
- Mucin 1 C-terminal subunit (MUC1-C) is an oncogenic protein aberrantly expressed in MM.
Purpose of the Study:
- To investigate the role of MUC1-C in regulating MYC expression in multiple myeloma.
- To elucidate the molecular mechanism by which MUC1-C influences MYC transcription.
Main Methods:
- Silencing of MUC1-C using CRISPR/Cas9 editing and the GO-203 inhibitor.
- Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) arrays.
- Analysis of microarray data from MM patient samples.
Main Results:
- MUC1-C silencing led to downregulation of MYC messenger RNA and protein.
- MUC1-C was found to occupy the MYC promoter, activating transcription via a β-catenin/TCF4 pathway.
- Silencing MUC1-C reduced the expression of MYC target genes (CCND2, hTERT, GCLC).
- MUC1 levels positively correlated with MYC expression in MM progression and patient samples.
Conclusions:
- MUC1-C drives MYC expression in multiple myeloma through a β-catenin/TCF4-mediated mechanism.
- Targeting MUC1-C represents a potential therapeutic strategy for MM by downregulating MYC.
- MUC1-C is a key regulator of MYC transcription in multiple myeloma.
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