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Published on: December 13, 2018
Long non-coding RNA LINC01003 suppresses the development of multiple myeloma by targeting miR-33a-5p/PIM1 axis
Linlin Wu1, Liang Xia1, Xiaowen Chen1
1Department of Hematology, The First Affiliated Hospital of Anhui Medical University, No. 218, Jixi Road, Shushan District, Hefei City, Anhui Province, 230032, China.
Background:
Numerous long non-coding RNAs (lncRNAs) are reported to affect the progression of multiple myeloma (MM). This study is aimed to explore the role and downstream mechanism of lncRNA LINC01003 in MM.
Materials And Methods:
Xenograft tumor assay was used to assess the function of LINC01003 in MM in vivo. The mRNA expression levels of LINC01003, miR-33a-5p, and PIM1 were determined by quantitative real-time polymerase chain reaction. Cell viability was examined by MTT assay. Relative protein levels of apoptosis-related factors (Bcl-2 and Bax) and proviral integration site of the Moloney leukemia virus kinase 1 (PIM1) were detected via western blot. Adhesion-related proteins were measured by Enzyme-linked immunosorbent assay was used to determine the levels of adhesion-related proteins. Besides, the target relation among LINC01003, miR-33a-5p and PIM1 was tested via dual-luciferase reporter assay.
Results:
Low expression of LINC01003 was observed in MM cell lines and peripheral blood samples of MM patients. Both LINC01003 up-regulation and miR-33a-5p down-regulation repressed cell viability and adhesion, and promoted apoptosis of MM cells. Moreover, LINC01003 suppressed the growth of xenograft tumor in mice. We then identified miR-33a-5p as a downstream target of LINC01003, and confirmed that PIM1 was a direct target gene of miR-33a-5p. Both high expression of miR-33a-5p and low expression of PIM1 reversed the suppressive effects of LINC01003 overexpression on cell adhesion and viability, and the promoting effect on apoptosis in MM cells.
Conclusion:
LINC01003 functioned as a sponge of miR-33a-5p to inhibit the development MM by regulating PIM1 expression.
Insights
This study reveals that long non-coding RNA LINC01003 inhibits multiple myeloma (MM) progression by acting as a sponge for miR-33a-5p, thereby regulating PIM1 expression and impacting cell viability and apoptosis.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Multiple myeloma (MM) progression is influenced by numerous long non-coding RNAs (lncRNAs).
- Understanding the specific roles and mechanisms of individual lncRNAs in MM is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of lncRNA LINC01003 in the progression of multiple myeloma (MM).
- To elucidate the downstream molecular mechanism through which LINC01003 exerts its effects in MM.
Main Methods:
- Quantitative real-time PCR and western blot were used to measure gene and protein expression levels.
- Cell viability, apoptosis, and adhesion assays (MTT, western blot, ELISA) were performed.
- In vivo studies utilized xenograft tumor models in mice.
- Dual-luciferase reporter assays confirmed the targeting relationship between LINC01003, miR-33a-5p, and PIM1.
Main Results:
- LINC01003 was found to be lowly expressed in MM cell lines and patient samples.
- Overexpression of LINC01003 suppressed MM cell viability and adhesion while promoting apoptosis.
- LINC01003 acts as a molecular sponge for miR-33a-5p, and PIM1 is a direct target of miR-33a-5p.
Conclusions:
- LINC01003 inhibits MM development by sponging miR-33a-5p and consequently regulating PIM1 expression.
- LINC01003 demonstrates potential as a therapeutic target for multiple myeloma.
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