NOD2 silencing promotes cell apoptosis and inhibits drug resistance in chronic lymphocytic leukemia by inhibiting the NF-κB signaling pathway
Recent years have witnessed increasing studies on the effect of epigenetic silencing of genes in the progression of chronic lymphocytic leukemia (CLL). This study investigates whether the nucleotide binding oligomerization domain containing 2 (NOD2) participates in the cell apoptosis and drug resist...
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| Veröffentlicht in: | Journal of biochemical and molecular toxicology 2023-12, Vol.37 (12), p.e23510-e23510 |
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| container_title | Journal of biochemical and molecular toxicology |
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| creator | Zheng, Cuiping Zhu, Zongsi Weng, Shanshan Zhang, Qikai Fu, Yixiao Cai, Xiaoping Liu, Zhen Shi, Yuejian |
| description | Recent years have witnessed increasing studies on the effect of epigenetic silencing of genes in the progression of chronic lymphocytic leukemia (CLL). This study investigates whether the nucleotide binding oligomerization domain containing 2 (NOD2) participates in the cell apoptosis and drug resistance of CLL cells. Cells were treated with adriamycin (ADR), etoposide, aclacinomycin and daunorubicin. After treatment, drug resistance and cell proliferation were examined to detect the inhibitory effect of ADR on cell proliferation; flow cytometry to identify ADR accumulation, the cell cycle distribution and apoptosis after transfection, and rhodamine 123 accumulation and efflux tests to assess P-glycoprotein (P-gp) function. NOD2 silencing or inhibition of the nuclear factor kappa-B (NF-κB) signaling pathway suppressed the multidrug resistance level in CLL, the inhibition rate, and cell proliferation caused by ADR at concentrations of approximately 0.25-1.5 μmol/L. Greater accumulation of ADR was observed in the CLL-AAT cell line than in the CLL-AAT/A02 cell line, but NOD2 silencing or inhibition of the NF-κB signaling pathway further increased the accumulation of ADR drugs in the CLL-AAT cell line and inhibited the drug efflux pump function of P-gp. Additionally, NOD2 silencing or NF-κB signaling pathway inhibition increased the apoptotic rate. The results of this study indicate that NOD2 promotes cell apoptosis and reduces the drug resistance of CLL by inhibiting the NF-κB signaling pathway. |
| doi_str_mv | 10.1002/jbt.23510 |
| format | Article |
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This study investigates whether the nucleotide binding oligomerization domain containing 2 (NOD2) participates in the cell apoptosis and drug resistance of CLL cells. Cells were treated with adriamycin (ADR), etoposide, aclacinomycin and daunorubicin. After treatment, drug resistance and cell proliferation were examined to detect the inhibitory effect of ADR on cell proliferation; flow cytometry to identify ADR accumulation, the cell cycle distribution and apoptosis after transfection, and rhodamine 123 accumulation and efflux tests to assess P-glycoprotein (P-gp) function. NOD2 silencing or inhibition of the nuclear factor kappa-B (NF-κB) signaling pathway suppressed the multidrug resistance level in CLL, the inhibition rate, and cell proliferation caused by ADR at concentrations of approximately 0.25-1.5 μmol/L. Greater accumulation of ADR was observed in the CLL-AAT cell line than in the CLL-AAT/A02 cell line, but NOD2 silencing or inhibition of the NF-κB signaling pathway further increased the accumulation of ADR drugs in the CLL-AAT cell line and inhibited the drug efflux pump function of P-gp. Additionally, NOD2 silencing or NF-κB signaling pathway inhibition increased the apoptotic rate. The results of this study indicate that NOD2 promotes cell apoptosis and reduces the drug resistance of CLL by inhibiting the NF-κB signaling pathway.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.23510</identifier><identifier>PMID: 37700718</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Accumulation ; Apoptosis ; ATP Binding Cassette Transporter, Subfamily B - metabolism ; ATP Binding Cassette Transporter, Subfamily B, Member 1 ; Cell cycle ; Cell growth ; Cell proliferation ; Chronic lymphocytic leukemia ; Daunorubicin ; Doxorubicin - pharmacology ; Doxorubicin - therapeutic use ; Drug resistance ; Drug Resistance, Neoplasm ; Efflux ; Epigenetics ; Etoposide ; Flow cytometry ; Gene silencing ; Glycoproteins ; Humans ; Leukemia ; Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell - genetics ; Leukemia, Lymphocytic, Chronic, B-Cell - metabolism ; Multidrug resistance ; NF-kappa B - metabolism ; NOD2 protein ; Nod2 Signaling Adaptor Protein - genetics ; Nod2 Signaling Adaptor Protein - metabolism ; Nod2 Signaling Adaptor Protein - pharmacology ; Nucleotides ; Oligomerization ; Rhodamine ; Signal Transduction ; Transfection</subject><ispartof>Journal of biochemical and molecular toxicology, 2023-12, Vol.37 (12), p.e23510-e23510</ispartof><rights>2023 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c273t-96ac3b61bda51da4076623d9ea3b146afd6aba773e75dab566d7c1c05712ae2d3</cites><orcidid>0000-0002-9758-9098 ; 0000-0003-0112-7321</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37700718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Cuiping</creatorcontrib><creatorcontrib>Zhu, Zongsi</creatorcontrib><creatorcontrib>Weng, Shanshan</creatorcontrib><creatorcontrib>Zhang, Qikai</creatorcontrib><creatorcontrib>Fu, Yixiao</creatorcontrib><creatorcontrib>Cai, Xiaoping</creatorcontrib><creatorcontrib>Liu, Zhen</creatorcontrib><creatorcontrib>Shi, Yuejian</creatorcontrib><title>NOD2 silencing promotes cell apoptosis and inhibits drug resistance in chronic lymphocytic leukemia by inhibiting the NF-κB signaling pathway</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Recent years have witnessed increasing studies on the effect of epigenetic silencing of genes in the progression of chronic lymphocytic leukemia (CLL). This study investigates whether the nucleotide binding oligomerization domain containing 2 (NOD2) participates in the cell apoptosis and drug resistance of CLL cells. Cells were treated with adriamycin (ADR), etoposide, aclacinomycin and daunorubicin. After treatment, drug resistance and cell proliferation were examined to detect the inhibitory effect of ADR on cell proliferation; flow cytometry to identify ADR accumulation, the cell cycle distribution and apoptosis after transfection, and rhodamine 123 accumulation and efflux tests to assess P-glycoprotein (P-gp) function. NOD2 silencing or inhibition of the nuclear factor kappa-B (NF-κB) signaling pathway suppressed the multidrug resistance level in CLL, the inhibition rate, and cell proliferation caused by ADR at concentrations of approximately 0.25-1.5 μmol/L. Greater accumulation of ADR was observed in the CLL-AAT cell line than in the CLL-AAT/A02 cell line, but NOD2 silencing or inhibition of the NF-κB signaling pathway further increased the accumulation of ADR drugs in the CLL-AAT cell line and inhibited the drug efflux pump function of P-gp. Additionally, NOD2 silencing or NF-κB signaling pathway inhibition increased the apoptotic rate. The results of this study indicate that NOD2 promotes cell apoptosis and reduces the drug resistance of CLL by inhibiting the NF-κB signaling pathway.</description><subject>Accumulation</subject><subject>Apoptosis</subject><subject>ATP Binding Cassette Transporter, Subfamily B - metabolism</subject><subject>ATP Binding Cassette Transporter, Subfamily B, Member 1</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chronic lymphocytic leukemia</subject><subject>Daunorubicin</subject><subject>Doxorubicin - pharmacology</subject><subject>Doxorubicin - therapeutic use</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Efflux</subject><subject>Epigenetics</subject><subject>Etoposide</subject><subject>Flow cytometry</subject><subject>Gene silencing</subject><subject>Glycoproteins</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - metabolism</subject><subject>Multidrug resistance</subject><subject>NF-kappa B - metabolism</subject><subject>NOD2 protein</subject><subject>Nod2 Signaling Adaptor Protein - genetics</subject><subject>Nod2 Signaling Adaptor Protein - metabolism</subject><subject>Nod2 Signaling Adaptor Protein - pharmacology</subject><subject>Nucleotides</subject><subject>Oligomerization</subject><subject>Rhodamine</subject><subject>Signal Transduction</subject><subject>Transfection</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUtu3DAMhoWiQd6LXiAQ0E2zcCJZtjReNtOmDRDMbJK1QT1mrIltuZKMwpfogXqInqny5LHIigT1kb_IH6FPlFxRQvLrnYxXOSsp-YCOKamqjBScftznZca5IEfoJIQdIaSsRHmIjpgQhAi6OEZ_VutvOQ62Nb2y_RYP3nUumoCVaVsMgxuiCzZg6DW2fWOljQFrP26xN6keoVcmPWDVeNdbhdupGxqnpjjnZnwynQUsp9feWSI2Bq9us39_b5Lutod2rwux-Q3TGTrYQBvM-Us8RY-33x-WP7P79Y-75df7TOWCxazioJjkVGooqYaCCM5zpisDTNKCw0ZzkCAEM6LUIEvOtVBUkVLQHEyu2Sn68jw37ftrNCHWnQ3zytAbN4Y6X_B0wkVBWEI_v0N3bvTp2zNVVYxWxYIm6vKZUt6F4M2mHrztwE81JfVsUp1MqvcmJfbiZeIoO6PfyFdX2H9QOY_G</recordid><startdate>202312</startdate><enddate>202312</enddate><creator>Zheng, Cuiping</creator><creator>Zhu, Zongsi</creator><creator>Weng, Shanshan</creator><creator>Zhang, Qikai</creator><creator>Fu, Yixiao</creator><creator>Cai, Xiaoping</creator><creator>Liu, Zhen</creator><creator>Shi, Yuejian</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9758-9098</orcidid><orcidid>https://orcid.org/0000-0003-0112-7321</orcidid></search><sort><creationdate>202312</creationdate><title>NOD2 silencing promotes cell apoptosis and inhibits drug resistance in chronic lymphocytic leukemia by inhibiting the NF-κB signaling pathway</title><author>Zheng, Cuiping ; Zhu, Zongsi ; Weng, Shanshan ; Zhang, Qikai ; Fu, Yixiao ; Cai, Xiaoping ; Liu, Zhen ; Shi, Yuejian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c273t-96ac3b61bda51da4076623d9ea3b146afd6aba773e75dab566d7c1c05712ae2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Accumulation</topic><topic>Apoptosis</topic><topic>ATP Binding Cassette Transporter, Subfamily B - metabolism</topic><topic>ATP Binding Cassette Transporter, Subfamily B, Member 1</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Chronic lymphocytic leukemia</topic><topic>Daunorubicin</topic><topic>Doxorubicin - pharmacology</topic><topic>Doxorubicin - therapeutic use</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Efflux</topic><topic>Epigenetics</topic><topic>Etoposide</topic><topic>Flow cytometry</topic><topic>Gene silencing</topic><topic>Glycoproteins</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - metabolism</topic><topic>Multidrug resistance</topic><topic>NF-kappa B - metabolism</topic><topic>NOD2 protein</topic><topic>Nod2 Signaling Adaptor Protein - genetics</topic><topic>Nod2 Signaling Adaptor Protein - metabolism</topic><topic>Nod2 Signaling Adaptor Protein - pharmacology</topic><topic>Nucleotides</topic><topic>Oligomerization</topic><topic>Rhodamine</topic><topic>Signal Transduction</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Cuiping</creatorcontrib><creatorcontrib>Zhu, Zongsi</creatorcontrib><creatorcontrib>Weng, Shanshan</creatorcontrib><creatorcontrib>Zhang, Qikai</creatorcontrib><creatorcontrib>Fu, Yixiao</creatorcontrib><creatorcontrib>Cai, Xiaoping</creatorcontrib><creatorcontrib>Liu, Zhen</creatorcontrib><creatorcontrib>Shi, Yuejian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Cuiping</au><au>Zhu, Zongsi</au><au>Weng, Shanshan</au><au>Zhang, Qikai</au><au>Fu, Yixiao</au><au>Cai, Xiaoping</au><au>Liu, Zhen</au><au>Shi, Yuejian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NOD2 silencing promotes cell apoptosis and inhibits drug resistance in chronic lymphocytic leukemia by inhibiting the NF-κB signaling pathway</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2023-12</date><risdate>2023</risdate><volume>37</volume><issue>12</issue><spage>e23510</spage><epage>e23510</epage><pages>e23510-e23510</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Recent years have witnessed increasing studies on the effect of epigenetic silencing of genes in the progression of chronic lymphocytic leukemia (CLL). This study investigates whether the nucleotide binding oligomerization domain containing 2 (NOD2) participates in the cell apoptosis and drug resistance of CLL cells. Cells were treated with adriamycin (ADR), etoposide, aclacinomycin and daunorubicin. After treatment, drug resistance and cell proliferation were examined to detect the inhibitory effect of ADR on cell proliferation; flow cytometry to identify ADR accumulation, the cell cycle distribution and apoptosis after transfection, and rhodamine 123 accumulation and efflux tests to assess P-glycoprotein (P-gp) function. NOD2 silencing or inhibition of the nuclear factor kappa-B (NF-κB) signaling pathway suppressed the multidrug resistance level in CLL, the inhibition rate, and cell proliferation caused by ADR at concentrations of approximately 0.25-1.5 μmol/L. Greater accumulation of ADR was observed in the CLL-AAT cell line than in the CLL-AAT/A02 cell line, but NOD2 silencing or inhibition of the NF-κB signaling pathway further increased the accumulation of ADR drugs in the CLL-AAT cell line and inhibited the drug efflux pump function of P-gp. Additionally, NOD2 silencing or NF-κB signaling pathway inhibition increased the apoptotic rate. The results of this study indicate that NOD2 promotes cell apoptosis and reduces the drug resistance of CLL by inhibiting the NF-κB signaling pathway.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37700718</pmid><doi>10.1002/jbt.23510</doi><orcidid>https://orcid.org/0000-0002-9758-9098</orcidid><orcidid>https://orcid.org/0000-0003-0112-7321</orcidid></addata></record> |
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| subjects | Accumulation Apoptosis ATP Binding Cassette Transporter, Subfamily B - metabolism ATP Binding Cassette Transporter, Subfamily B, Member 1 Cell cycle Cell growth Cell proliferation Chronic lymphocytic leukemia Daunorubicin Doxorubicin - pharmacology Doxorubicin - therapeutic use Drug resistance Drug Resistance, Neoplasm Efflux Epigenetics Etoposide Flow cytometry Gene silencing Glycoproteins Humans Leukemia Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy Leukemia, Lymphocytic, Chronic, B-Cell - genetics Leukemia, Lymphocytic, Chronic, B-Cell - metabolism Multidrug resistance NF-kappa B - metabolism NOD2 protein Nod2 Signaling Adaptor Protein - genetics Nod2 Signaling Adaptor Protein - metabolism Nod2 Signaling Adaptor Protein - pharmacology Nucleotides Oligomerization Rhodamine Signal Transduction Transfection |
| title | NOD2 silencing promotes cell apoptosis and inhibits drug resistance in chronic lymphocytic leukemia by inhibiting the NF-κB signaling pathway |
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