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Updated: Jun 12, 2026
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Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model
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MYC-Mediated USP39 Upregulation Stabilizes SRSF1 in Pancreatic Cancer
Benteng Ma1, Xin Zhang1, Alexander J Kral2
1Stony Brook University Stony Brook, NY United States.
Molecular Cancer Research : MCR
|June 11, 2026
Summary
Researchers found that USP39 stabilizes SRSF1 protein, promoting pancreatic cancer progression. This discovery highlights a new MYC-USP39-SRSF1 pathway and identifies USP39 as a potential therapeutic target for pancreatic ductal adenocarcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer driven by KRAS signaling.
- The splicing factor SRSF1 is oncogenic in PDAC, but its stability regulation is unclear.
Purpose of the Study:
- To identify regulators of SRSF1 protein stability in PDAC.
- To elucidate the functional role and regulatory mechanisms of USP39 in PDAC.
Main Methods:
- Protein interaction assays to study USP39 and SRSF1.
- Ubiquitination assays to assess SRSF1 stability.
- Analysis of USP39 expression in PDAC patient data.
- Investigating MYC's role in USP39 transcription.
Main Results:
- USP39 directly interacts with SRSF1, suppressing its ubiquitination and stabilizing its levels.
- USP39 is upregulated in PDAC and linked to poor prognosis.
- USP39 promotes PDAC cell progression by stabilizing SRSF1.
- MYC transcriptionally activates USP39 via promoter binding.
Conclusions:
- A MYC-USP39-SRSF1 regulatory axis integrates transcriptional and post-translational control in PDAC.
- USP39 is a key regulator of PDAC progression and a potential therapeutic target.
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