Transcription of WNT Genes in Hematopoietic Niche's Mesenchymal Stem Cells in Multiple Myeloma Patients with Different Responses to Treatment
Mesenchymal stromal cells (MSCs) are involved in bone tissue remodeling due to their ability to differentiate into osteoblasts and to influence osteoclasts' activity. Multiple myeloma (MM) is associated with bone resorption. During disease progression, MSCs acquire a tumor-associated phenotype,...
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creator | Enukashvily, Natella I Belik, Liubov A Semenova, Natalia Yu Kostroma, Ivan I Motyko, Ekaterina V Gritsaev, Sergey V Bessmeltsev, Stanislav S Sidorkevich, Sergey V Martynkevich, Irina S |
description | Mesenchymal stromal cells (MSCs) are involved in bone tissue remodeling due to their ability to differentiate into osteoblasts and to influence osteoclasts' activity. Multiple myeloma (MM) is associated with bone resorption. During disease progression, MSCs acquire a tumor-associated phenotype, losing their osteogenic potential. The process is associated with impaired osteoblasts/osteoclasts balance. The WNT signaling pathway plays a major role in maintaining the balance. In MM, it functions in an aberrant way. It is not known yet whether the WNT pathway is restored in patients' bone narrow after treatment. The aim of the study was to compare the level of
family gene transcription in the bone marrow MSCs of healthy donors and MM patients before and after therapy. The study included healthy donors (
= 3), primary patients (
= 3) and patients with different response status to therapy (bortezomib-containing induction regimens) (
= 12). The transcription of the
and
(encoding β-catenin) genes was accessed using qPCR. The mRNA quantity of ten
genes, as well as
mRNA encoding β-catenin, a key mediator in canonical signaling, was evaluated. The observed differences between the groups of patients indicated that aberrant functioning of the WNT pathway was retained after treatment. The differences that we detected for
,
and
suggested their possible application as prognostic molecular markers. |
doi_str_mv | 10.3390/genes14051097 |
format | Article |
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family gene transcription in the bone marrow MSCs of healthy donors and MM patients before and after therapy. The study included healthy donors (
= 3), primary patients (
= 3) and patients with different response status to therapy (bortezomib-containing induction regimens) (
= 12). The transcription of the
and
(encoding β-catenin) genes was accessed using qPCR. The mRNA quantity of ten
genes, as well as
mRNA encoding β-catenin, a key mediator in canonical signaling, was evaluated. The observed differences between the groups of patients indicated that aberrant functioning of the WNT pathway was retained after treatment. The differences that we detected for
,
and
suggested their possible application as prognostic molecular markers.</description><identifier>ISSN: 2073-4425</identifier><identifier>EISSN: 2073-4425</identifier><identifier>DOI: 10.3390/genes14051097</identifier><identifier>PMID: 37239457</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>beta Catenin - genetics ; beta Catenin - metabolism ; Bone remodeling ; Bone resorption ; Bortezomib ; Cancer ; Cell culture ; Cell Differentiation - physiology ; Cell growth ; Genes ; Humans ; Ligands ; Mesenchymal stem cells ; Mesenchymal Stem Cells - metabolism ; Multiple myeloma ; Multiple Myeloma - genetics ; Multiple Myeloma - therapy ; Osteoblasts ; Osteoclasts ; Phenotypes ; Proteins ; Remission (Medicine) ; RNA, Messenger - genetics ; Signal transduction ; Stem cells ; Stromal cells ; Transcription ; Wnt protein ; Wnt Signaling Pathway - genetics ; β-Catenin</subject><ispartof>Genes, 2023-05, Vol.14 (5), p.1097</ispartof><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c372t-8d17e0cce5d23cfa017e788c997987f02aad6e5c658e3eda60003138547b66383</cites><orcidid>0000-0002-5971-7917 ; 0000-0002-4589-8702 ; 0000-0003-3768-0831 ; 0000-0003-4069-0678 ; 0000-0001-7586-4709</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10218155/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10218155/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37239457$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Enukashvily, Natella I</creatorcontrib><creatorcontrib>Belik, Liubov A</creatorcontrib><creatorcontrib>Semenova, Natalia Yu</creatorcontrib><creatorcontrib>Kostroma, Ivan I</creatorcontrib><creatorcontrib>Motyko, Ekaterina V</creatorcontrib><creatorcontrib>Gritsaev, Sergey V</creatorcontrib><creatorcontrib>Bessmeltsev, Stanislav S</creatorcontrib><creatorcontrib>Sidorkevich, Sergey V</creatorcontrib><creatorcontrib>Martynkevich, Irina S</creatorcontrib><title>Transcription of WNT Genes in Hematopoietic Niche's Mesenchymal Stem Cells in Multiple Myeloma Patients with Different Responses to Treatment</title><title>Genes</title><addtitle>Genes (Basel)</addtitle><description>Mesenchymal stromal cells (MSCs) are involved in bone tissue remodeling due to their ability to differentiate into osteoblasts and to influence osteoclasts' activity. Multiple myeloma (MM) is associated with bone resorption. During disease progression, MSCs acquire a tumor-associated phenotype, losing their osteogenic potential. The process is associated with impaired osteoblasts/osteoclasts balance. The WNT signaling pathway plays a major role in maintaining the balance. In MM, it functions in an aberrant way. It is not known yet whether the WNT pathway is restored in patients' bone narrow after treatment. The aim of the study was to compare the level of
family gene transcription in the bone marrow MSCs of healthy donors and MM patients before and after therapy. The study included healthy donors (
= 3), primary patients (
= 3) and patients with different response status to therapy (bortezomib-containing induction regimens) (
= 12). The transcription of the
and
(encoding β-catenin) genes was accessed using qPCR. The mRNA quantity of ten
genes, as well as
mRNA encoding β-catenin, a key mediator in canonical signaling, was evaluated. The observed differences between the groups of patients indicated that aberrant functioning of the WNT pathway was retained after treatment. The differences that we detected for
,
and
suggested their possible application as prognostic molecular markers.</description><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Bone remodeling</subject><subject>Bone resorption</subject><subject>Bortezomib</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Cell Differentiation - physiology</subject><subject>Cell growth</subject><subject>Genes</subject><subject>Humans</subject><subject>Ligands</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Multiple myeloma</subject><subject>Multiple Myeloma - genetics</subject><subject>Multiple Myeloma - therapy</subject><subject>Osteoblasts</subject><subject>Osteoclasts</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Remission (Medicine)</subject><subject>RNA, Messenger - genetics</subject><subject>Signal transduction</subject><subject>Stem cells</subject><subject>Stromal cells</subject><subject>Transcription</subject><subject>Wnt protein</subject><subject>Wnt Signaling Pathway - genetics</subject><subject>β-Catenin</subject><issn>2073-4425</issn><issn>2073-4425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkU1PFTEUhhuiAXJlydY0caGb0X5Mp52VMVcFEy4SuIRlUzpnuCUz7dh2NPdH-J8tggTspj2nT97z8SJ0SMl7zlvy4QY8JFoTQUkrd9A-I5JXdc3EiyfvPXSQ0i0ppyaMELGL9rhkvK2F3Ee_19H4ZKObsgsehx5fna7x0Z0udh4fw2hymIKD7Cw-dXYDbxNeQQJvN9vRDPgiw4iXMAx_-dU8ZDcNgFdbGMJo8JnJDnxO-JfLG_zZ9T3EEuNzSFPwqVTJAa8jmDyW9Cv0sjdDgoOHe4Euv35ZL4-rk-9H35afTipbOs-V6qgEYi2IjnHbG1JCqZRtW9kq2RNmTNeAsI1QwKEzTZmdU65ELa-bhiu-QB_vdaf5eoTOltLRDHqKbjRxq4Nx-vmPdxt9E35qShhVVIii8O5BIYYfM6SsR5dsWYPxEOakmSqrpg0vJizQm__Q2zBHX-YrFG3rWjWCFaq6p2wMKUXoH7uhRN-ZrZ-ZXfjXT0d4pP9Zy_8AFiSneA</recordid><startdate>20230517</startdate><enddate>20230517</enddate><creator>Enukashvily, Natella I</creator><creator>Belik, Liubov A</creator><creator>Semenova, Natalia Yu</creator><creator>Kostroma, Ivan I</creator><creator>Motyko, Ekaterina V</creator><creator>Gritsaev, Sergey V</creator><creator>Bessmeltsev, Stanislav S</creator><creator>Sidorkevich, Sergey V</creator><creator>Martynkevich, Irina S</creator><general>MDPI AG</general><general>MDPI</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>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5971-7917</orcidid><orcidid>https://orcid.org/0000-0002-4589-8702</orcidid><orcidid>https://orcid.org/0000-0003-3768-0831</orcidid><orcidid>https://orcid.org/0000-0003-4069-0678</orcidid><orcidid>https://orcid.org/0000-0001-7586-4709</orcidid></search><sort><creationdate>20230517</creationdate><title>Transcription of WNT Genes in Hematopoietic Niche's Mesenchymal Stem Cells in Multiple Myeloma Patients with Different Responses to Treatment</title><author>Enukashvily, Natella I ; Belik, Liubov A ; Semenova, Natalia Yu ; Kostroma, Ivan I ; Motyko, Ekaterina V ; Gritsaev, Sergey V ; Bessmeltsev, Stanislav S ; Sidorkevich, Sergey V ; Martynkevich, Irina S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-8d17e0cce5d23cfa017e788c997987f02aad6e5c658e3eda60003138547b66383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Bone remodeling</topic><topic>Bone resorption</topic><topic>Bortezomib</topic><topic>Cancer</topic><topic>Cell culture</topic><topic>Cell Differentiation - physiology</topic><topic>Cell growth</topic><topic>Genes</topic><topic>Humans</topic><topic>Ligands</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Multiple myeloma</topic><topic>Multiple Myeloma - genetics</topic><topic>Multiple Myeloma - therapy</topic><topic>Osteoblasts</topic><topic>Osteoclasts</topic><topic>Phenotypes</topic><topic>Proteins</topic><topic>Remission (Medicine)</topic><topic>RNA, Messenger - genetics</topic><topic>Signal transduction</topic><topic>Stem cells</topic><topic>Stromal cells</topic><topic>Transcription</topic><topic>Wnt protein</topic><topic>Wnt Signaling Pathway - genetics</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Enukashvily, Natella I</creatorcontrib><creatorcontrib>Belik, Liubov A</creatorcontrib><creatorcontrib>Semenova, Natalia Yu</creatorcontrib><creatorcontrib>Kostroma, Ivan I</creatorcontrib><creatorcontrib>Motyko, Ekaterina V</creatorcontrib><creatorcontrib>Gritsaev, Sergey V</creatorcontrib><creatorcontrib>Bessmeltsev, Stanislav S</creatorcontrib><creatorcontrib>Sidorkevich, Sergey V</creatorcontrib><creatorcontrib>Martynkevich, Irina S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Enukashvily, Natella I</au><au>Belik, Liubov A</au><au>Semenova, Natalia Yu</au><au>Kostroma, Ivan I</au><au>Motyko, Ekaterina V</au><au>Gritsaev, Sergey V</au><au>Bessmeltsev, Stanislav S</au><au>Sidorkevich, Sergey V</au><au>Martynkevich, Irina S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcription of WNT Genes in Hematopoietic Niche's Mesenchymal Stem Cells in Multiple Myeloma Patients with Different Responses to Treatment</atitle><jtitle>Genes</jtitle><addtitle>Genes (Basel)</addtitle><date>2023-05-17</date><risdate>2023</risdate><volume>14</volume><issue>5</issue><spage>1097</spage><pages>1097-</pages><issn>2073-4425</issn><eissn>2073-4425</eissn><abstract>Mesenchymal stromal cells (MSCs) are involved in bone tissue remodeling due to their ability to differentiate into osteoblasts and to influence osteoclasts' activity. Multiple myeloma (MM) is associated with bone resorption. During disease progression, MSCs acquire a tumor-associated phenotype, losing their osteogenic potential. The process is associated with impaired osteoblasts/osteoclasts balance. The WNT signaling pathway plays a major role in maintaining the balance. In MM, it functions in an aberrant way. It is not known yet whether the WNT pathway is restored in patients' bone narrow after treatment. The aim of the study was to compare the level of
family gene transcription in the bone marrow MSCs of healthy donors and MM patients before and after therapy. The study included healthy donors (
= 3), primary patients (
= 3) and patients with different response status to therapy (bortezomib-containing induction regimens) (
= 12). The transcription of the
and
(encoding β-catenin) genes was accessed using qPCR. The mRNA quantity of ten
genes, as well as
mRNA encoding β-catenin, a key mediator in canonical signaling, was evaluated. The observed differences between the groups of patients indicated that aberrant functioning of the WNT pathway was retained after treatment. The differences that we detected for
,
and
suggested their possible application as prognostic molecular markers.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37239457</pmid><doi>10.3390/genes14051097</doi><orcidid>https://orcid.org/0000-0002-5971-7917</orcidid><orcidid>https://orcid.org/0000-0002-4589-8702</orcidid><orcidid>https://orcid.org/0000-0003-3768-0831</orcidid><orcidid>https://orcid.org/0000-0003-4069-0678</orcidid><orcidid>https://orcid.org/0000-0001-7586-4709</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | beta Catenin - genetics beta Catenin - metabolism Bone remodeling Bone resorption Bortezomib Cancer Cell culture Cell Differentiation - physiology Cell growth Genes Humans Ligands Mesenchymal stem cells Mesenchymal Stem Cells - metabolism Multiple myeloma Multiple Myeloma - genetics Multiple Myeloma - therapy Osteoblasts Osteoclasts Phenotypes Proteins Remission (Medicine) RNA, Messenger - genetics Signal transduction Stem cells Stromal cells Transcription Wnt protein Wnt Signaling Pathway - genetics β-Catenin |
title | Transcription of WNT Genes in Hematopoietic Niche's Mesenchymal Stem Cells in Multiple Myeloma Patients with Different Responses to Treatment |
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