miR-1248 enhances bortezomib-induced autophagy by targeting MEF2C/p38-MAPK signaling in multiple myeloma
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By
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Wei Wang
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Rong-juan Zhang
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Ming-shuai Ma
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Xiao-min Shi
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Qing Zhang
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Chong Li
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Zhi-hua Zhang
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Chang-lai Hao
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June 26, 2026
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Clinical Scorecard: miR-1248 promotes autophagy induced by bortezomib through modulation of MEF2C/p38-MAPK pathway in multiple myeloma
At a Glance
| Category | Detail |
|---|
| Condition | Multiple Myeloma |
| Key Mechanisms | miR-1248 enhances bortezomib sensitivity by targeting MEF2C and modulating p38-MAPK pathway. |
| Target Population | Patients with multiple myeloma undergoing bortezomib treatment. |
| Care Setting | Oncology, specifically in the context of chemotherapy resistance. |
Key Highlights
- miR-1248 is significantly upregulated in response to bortezomib treatment.
- Inhibition of miR-1248 reduces autophagy markers and restores MEF2C and p38 expression.
- Overexpression of MEF2C decreases bortezomib-induced apoptosis.
- miR-1248 knockdown in xenograft models reduces tumor inhibition.
- The study identifies a miR-1248–MEF2C–p38MAPK axis as a potential therapeutic target.
Guideline-Based Recommendations
Diagnosis
- Monitor miR-1248 levels in multiple myeloma patients to assess bortezomib sensitivity.
Management
- Consider targeting the miR-1248–MEF2C–p38MAPK pathway to improve bortezomib response.
Monitoring & Follow-up
- Evaluate autophagy markers and MEF2C expression in patients undergoing bortezomib therapy.
Risks
- Inhibition of miR-1248 may lead to reduced autophagic activity and increased tumor viability.
Patient & Prescribing Data
Newly diagnosed multiple myeloma patients receiving VCD chemotherapy.
Bortezomib treatment can modulate miR-1248 levels, impacting treatment outcomes.
Clinical Best Practices
- Utilize RNA-seq to identify miRNA profiles in multiple myeloma.
- Incorporate autophagy assessments in treatment planning for bortezomib therapy.
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