Evidence map›Paper›PMID 35117295›Full record

ArticleTranslational cancer research2020

Expression profiling analysis reveals molecular mechanism of Lnc00675 downregulation promoting cell apoptosis in acute myeloid leukemia U937 cells.

Miao Miao, Mengqi Li, Zhuogang Liu, Wei Yang, Chen Wang, Rong Hu

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Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Miao MiaoDepartment of Hematology, Shengjing Hospital, China Medical University, Shenyang, China.
Mengqi LiDepartment of Hematology, Shengjing Hospital, China Medical University, Shenyang, China.
Zhuogang LiuDepartment of Hematology, Shengjing Hospital, China Medical University, Shenyang, China.
Wei YangDepartment of Hematology, Shengjing Hospital, China Medical University, Shenyang, China.
Chen WangDepartment of Hematology, Shengjing Hospital, China Medical University, Shenyang, China.
Rong HuDepartment of Hematology, Shengjing Hospital, China Medical University, Shenyang, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML), an aggressive malignancy with poor prognosis, is the most common in adult leukemia. Long non-coding RNA (lncRNA) could affect the regulation of protein-coding genes, cell proliferation and apoptosis, tumor cell resistance to radio- and chemotherapy and pathological processes. Lnc00675 is a lncRNA also known as transmembrane protein 238 like (TMEM238L), which identified as a marker of tumor promoter and unfavorable prognosis in patients with pancreatic ductal adenocarcinoma, glioma and cervical cancer. However, the association between Lnc00675 and hematological tumors has not been previously reported.

methodsExpression profile gene chip technology was used to screen for differentially expressed genes (DEGs) through comparing Lnc00675 overexpression and Lnc00675 downregulation. Gene ontology (GO) analysis was performed to identify the biologic implications of the DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed to identify biologically important pathways associated with the DEGs. Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis were utilized to detect the cell proliferation rate and the cell apoptosis rate, respectively.

resultsComparing Lnc00675 overexpression and Lnc00675 downregulation, a total of 866 and 1,115 DEGs were upregulated and downregulated, respectively. Bioinformatics analysis indicated that Lnc00675 might affect U937 cells proliferation and apoptosis through JAK-STAT signaling pathway and PI3K-Akt signaling pathway. The cell proliferation rate in si-Lnc00675 group was significantly lower than those of si-NC group and Lnc00675 group (P<0.05). The cell apoptosis rate of si-Lnc00675 group (22.93%±2.24%) was significantly higher than those of si-NC group (0.37%±0.88%) and Lnc00675 group (0.73%±0.35%) (P<0.01).

conclusionsDownregulation of lnc00675 expression inhibited proliferation and promoted apoptosis in human leukemia U937 cells.

Indexed as

acute myeloid leukemia (AML)expression profile analysisJAK-STAT signaling pathwayLnc00675PI3K-Akt signaling pathwayU937 cells

Identifiers

PMID35117295
PMCPMC8798533
OpenAlexW3104272427

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