Contributions
Abstract: EP601
Type: E-Poster Presentation
Session title: Chronic lymphocytic leukemia and related disorders - Biology & Translational Research
Background
Emerging evidences have indicated that long noncoding RNAs (lncRNAs) play essential roles in the development and progression of cancers. LncRNAs were aberrantly expressed in most hematological malignancies including leukemia, participating in tumor suppression or promoting oncogenesis and modulating key genes in different pathways. Dysregulation of LINC00525 has recently been reported in several types of cancers, and researches on the function of LINC00525 in cancers suggested that LINC00525 could act as an oncogene. But the functional involvement of LINC00525 has not been studied in chronic lymphocytic leukemia (CLL).
Aims
In order to explore the expression and biological function of LINC00525 in CLL.
Methods
In our study, CCK8 assays, cycle assays, apotosis experiments were used to identify biological effects of LINC00525 on CLL cells in vitro. The expression of LINC00525, microRNA-338-3p (miR-338-3p) were detected by qRT-PCR. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to show the interactions of LINC00525 and miR-338-3p. The bioinformatics methods were completed to find the target genes of miR-338-3p. And Dual-luciferase reporter assay and Western blot analysis were further used to confirm the target gene of miR-338-3p.
Results
We found that LINC00525 knockdown obviously suppressed CLL proliferation and increase apoptosis in vitro. Besides, silencing of LINC00525 significantly increased the expression of microRNA-338-3p (miR-338-3p), which could play a tumor suppressor role in CLL. Moreover, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay revealed that LINC00525 exerted tumor-suppressive functions by binding directly to miR-338-3p, and there was a reciprocal inhibition between LINC00525 and miR-338-3p in the same RNA induced silencing complex (RISC). Furthermore, overexpression of LINC00525 enhanced the expression of suppression of the E3 ubiquitin ligase (E3) WWP1, which was identified as a downstream target gene of miR-338-3P. Thus, LINC00525 positively regulated WWP1 expression through sponging miR-338-3P, and acted as tumor suppressor in CLL.
Conclusion
LINC00525 promotes cell proliferation through LINC00525/miR-338-3p/ WWP1 axis in CLL.
Keyword(s): Chronic lymphocytic leukemia
Abstract: EP601
Type: E-Poster Presentation
Session title: Chronic lymphocytic leukemia and related disorders - Biology & Translational Research
Background
Emerging evidences have indicated that long noncoding RNAs (lncRNAs) play essential roles in the development and progression of cancers. LncRNAs were aberrantly expressed in most hematological malignancies including leukemia, participating in tumor suppression or promoting oncogenesis and modulating key genes in different pathways. Dysregulation of LINC00525 has recently been reported in several types of cancers, and researches on the function of LINC00525 in cancers suggested that LINC00525 could act as an oncogene. But the functional involvement of LINC00525 has not been studied in chronic lymphocytic leukemia (CLL).
Aims
In order to explore the expression and biological function of LINC00525 in CLL.
Methods
In our study, CCK8 assays, cycle assays, apotosis experiments were used to identify biological effects of LINC00525 on CLL cells in vitro. The expression of LINC00525, microRNA-338-3p (miR-338-3p) were detected by qRT-PCR. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to show the interactions of LINC00525 and miR-338-3p. The bioinformatics methods were completed to find the target genes of miR-338-3p. And Dual-luciferase reporter assay and Western blot analysis were further used to confirm the target gene of miR-338-3p.
Results
We found that LINC00525 knockdown obviously suppressed CLL proliferation and increase apoptosis in vitro. Besides, silencing of LINC00525 significantly increased the expression of microRNA-338-3p (miR-338-3p), which could play a tumor suppressor role in CLL. Moreover, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay revealed that LINC00525 exerted tumor-suppressive functions by binding directly to miR-338-3p, and there was a reciprocal inhibition between LINC00525 and miR-338-3p in the same RNA induced silencing complex (RISC). Furthermore, overexpression of LINC00525 enhanced the expression of suppression of the E3 ubiquitin ligase (E3) WWP1, which was identified as a downstream target gene of miR-338-3P. Thus, LINC00525 positively regulated WWP1 expression through sponging miR-338-3P, and acted as tumor suppressor in CLL.
Conclusion
LINC00525 promotes cell proliferation through LINC00525/miR-338-3p/ WWP1 axis in CLL.
Keyword(s): Chronic lymphocytic leukemia