The Experimental Study Of LINC00675 Affecting The Proliferation And Apoptosis Of Acute Myeloid Leukemia Cells

Objective: Acute myeloid leukemia(AML)is a hematological malignancy characterized by a low cure rate and high recurrence rate.Previous studies have shown that long noncoding RNA(lncRNA)may be an important pathogenic factor for AML.However,the biological role and clinical significance of most lncRNAs in AML are not fully understood.As a member of the lncRNA family,LINC00675 has little research on its function in AML.Methods: The targeted miRNA of LINC00675 and the corresponding m RNA of the targeted miRNA were predicted by DIANA-Lnc Base v3.0,Target Scan,miRDB and miRWalk databases.Quantitative reverse transcription-polymerase chain reaction(RTq PCR)was used to detect the expression of LINC00675 and CDK6 in AML.The effects of LINC00675 on the proliferation and apoptosis of AML cells were determined by CCK-8 test,flow cytometry and Western blot.In addition,the mechanism of LINC00675 promoting the occurrence and development of AML through miR-6809-CDK6 was explored through the double luciferase reporter gene experiment.Results: 1.The prediction results of the Lnc Locator database showed that the expression of LINC00675 in the cytoplasm was significantly higher than that in the nucleus.LINC00675 may affect the progression of AML through the ce RNA mechanism.2.According to the prediction results of DIANA-Lnc Base v3.0,Target Scan,miRDB and miRWalk databases,LINC00675 may participate in the progression of AML through the LINC00675-miR-6809-CDK6 axis.3.The enrichment analysis results showed that LINC00675 might affect cell proliferation,apoptosis and various cancer-related signal pathways.4.Immune infiltration analysis and drug sensitivity analysis showed that compared with patients with low expression of LINC00675,patients with high expression of LINC00675 had a higher expression level of most immune checkpoint-related genes and higher sensitivity to palbociclib.Immune checkpoint inhibitors and palbociclib may help to improve the prognosis of AML patients with high expression of LINC00675.5.RTq PCR results showed that LINC00675 and CDK6 were overexpressed in AML cell lines.6.The luciferase reporter assay showed that LINC00675 binds to miR-6809 and CDK6 to miR-6809.7.Knockdown of LINC00675 inhibited the proliferation of AML cells and promoted the apoptosis of AML cells.8.CCK-8 experiments,flow cytometry and Western blot proved that LINC00675 overexpression targeted the miR-6809-CDK6 regulatory axis which promoted proliferation and inhibited apoptosis.Conclusions: 1.Through bioinformatics analysis,LINC00675 is associated with multiple clinicopathological parameters and its expression in cytoplasm is significantly higher than that in nucleus.We predicted that LINC00675 may be involved in the progression of AML through the LINC00675-miR-6809-CDK6 axis by using bioinformatics analysis.For patients with high expression of LINC00675,immune checkpoint inhibitors and palbociclib may help improve prognosis.LINC00675 is significantly upregulated in AML cells.2.Knockdown of LINC00675 inhibited cell proliferation and promoted cell apoptosis.By sponging miR-6809,LINC00675 enhances CDK6 expression and regulates AML progression through the miR-6809-CDK6 axis.Therefore,LINC00675 may serve as a predictive biomarker of AML and as a promising therapeutic target.