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pmid:35706822

Long non-coding RNA (LncRNA) CHROMR promotes the expression of the CNNM1 gene by adsorbing hsa-miR-1299 to obtain drug resistance in diffuse large B lymphoma cells.

Mingyue Wang · Zhichao Miao · Hong Cen · Jiaxu He · Changyuan Wei

Translational cancer research · 2022 doi:10.21037/tcr-22-1087

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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title
Long non-coding RNA (LncRNA) CHROMR promotes the expression of the CNNM1 gene by adsorbing hsa-miR-1299 to obtain drug resistance in diffuse large B lymphoma cells.
doi
10.21037/tcr-22-1087
pmid
35706822
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[0]
Mingyue Wang
[1]
Zhichao Miao
[2]
Hong Cen
[3]
Jiaxu He
[4]
Changyuan Wei
journal
Translational cancer research
year
2022
abstract
Background: Long non-coding RNA (LncRNA) play roles in different diseases, LncRNA is differentially expressed in diffuse large B cell lines with varying degrees of resistance to rituximab. Methods: In the GEO database (GSE159852), we found that CHROMR (cholesterol induced regulator of metabolism RNA) may be differentially expressed in different rituximab-resistant diffuse large B lymphoma cell lines. We also verified the expression level in cell lines and verified the role of CHROMR in acquiring cell drug resistance through various biological function experiments. We predict that there may be a potential regulatory mechanism for CHROMR and validated it. Results: We found that CHROMR was differentially expressed in different rituximab-resistant cell lines. When the rituximab-sensitive cell line SU_DHL_4 was stimulated by rituximab, flow experiments demonstrated that overexpression of CHROMR could reduce the level of cell apoptosis and the proportion of arrested cells in the G2/M phase of the cell cycle. cck8 experiments demonstrated that overexpression of CHROMR increased cell proliferation. Western Blot (WB) experiments confirmed that overexpression of CHROMR reduced the expression of apoptosis-related proteins. Dual-luciferase and recovery experiments suggested that CHROMR acted through the CHROMR/hsa-miR-1299/CNNM1 pathway. Conclusions: lncRNA CHROMR promotes the expression of the CNNM1 gene by adsorbing hsa-miR-1299 to obtain drug resistance in diffuse large B lymphoma cells.
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lncRNA CHROMR promotes the expression of the CNNM1 gene by adsorbing hsa-miR-1299 to obtain drug resistance in diffuse large B lymphoma cells.
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Long noncoding RNA expression in rituximab-sensitive and -resistant diffuse large B-cell lymphoma cell lines
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ion of CHROMR could reduce the level of cell apoptosis and the proportion of arrested cells in the
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Complete file
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We also verified the expression level in cell lines and verified the role of CHROMR in acquiring cell drug resistance through various biological function experiments. We predict that there may be a potential regulatory mechanism for CHROMR and validated it.\nResults: We found that CHROMR was differentially expressed in different rituximab-resistant cell lines. When the rituximab-sensitive cell line SU_DHL_4 was stimulated by rituximab, flow experiments demonstrated that overexpression of CHROMR could reduce the level of cell apoptosis and the proportion of arrested cells in the G2/M phase of the cell cycle. cck8 experiments demonstrated that overexpression of CHROMR increased cell proliferation. Western Blot (WB) experiments confirmed that overexpression of CHROMR reduced the expression of apoptosis-related proteins. 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