MYC-dependent MiR-7-5p regulated apoptosis and autophagy in diffuse large B cell lymphoma by targeting AMBRA1
2024

Role of miR-7-5p in Diffuse Large B-Cell Lymphoma

Sample size: 16 publication 10 minutes Evidence: moderate

Author Information

Author(s): Zhang Cuifen, Wang Ke, Tao Jiahao, Zheng Chuangjie, Zhai Linzhu

Primary Institution: Guangzhou University of Chinese Medicine

Hypothesis

This study investigates whether miR-7-5p regulates AMBRA1 and its effects on autophagy and apoptosis in diffuse large B-cell lymphoma (DLBCL).

Conclusion

The study concludes that miR-7-5p suppresses autophagy and apoptosis in DLBCL by targeting AMBRA1.

Supporting Evidence

  • MiR-7-5p was found to be upregulated in DLBCL cells.
  • Luciferase reporter assays confirmed AMBRA1 as a target of miR-7-5p.
  • Overexpression of miR-7-5p decreased apoptosis in DLBCL cells.
  • Silencing AMBRA1 led to increased apoptosis and decreased autophagy.
  • Hydroxychloroquine, an autophagy inhibitor, increased apoptosis in DLBCL cells.
  • In vivo experiments showed that miR-7-5p overexpression increased tumor volume and weight.
  • MiR-7-5p and c-MYC were found to have a positive feedback loop.

Takeaway

Researchers found that a tiny molecule called miR-7-5p can help cancer cells survive by stopping them from dying, which could be important for treating a type of blood cancer.

Methodology

The study used quantitative real-time PCR, transfection of miRNA mimics and inhibitors, dual-luciferase reporter assays, immunofluorescence, flow cytometry, and western blotting to assess the effects of miR-7-5p on autophagy and apoptosis.

Limitations

The study did not assess miR-7-5p levels in clinical DLBCL samples for further validation.

Participant Demographics

Sixteen female SCID mice were used in the in vivo experiments.

Statistical Information

P-Value

p<0.001

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1007/s11010-024-04946-w

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication