Inhibition of apoptosis may lead to the development of bortezomib resistance in multiple myeloma cancer cells
| dc.authorid | 0000-0003-4106-1056 | |
| dc.authorid | 0000-0002-2928-6474 | |
| dc.contributor.author | Öksüzoğlu, Emine | |
| dc.contributor.author | Kozalak, Gül | |
| dc.date.accessioned | 2021-05-25T07:45:29Z | |
| dc.date.available | 2021-05-25T07:45:29Z | |
| dc.date.issued | 2021 | |
| dc.department | Sabire Yazıcı Fen Edebiyat Fakültesi | |
| dc.description.abstract | Background: Multiple myeloma (MM), a malignancy of plasma cells, is the second most prevalent hematological cancer. Bortezomib is the most effective chemotherapeutic drug used in treatment. However, drug-resistance prevents success of chemotherapy. One of the factors causing drug-resistance is dysfunction of apoptotic-pathways. This study aimed to evaluate the relationship between expression levels of Bcl-2, Bax, caspase-3 and p-53 genes involved in apoptosis and the development of bortezomib-resistance in MM cell lines. Materials and methods: Multiple myeloma KMS20 (bortezomib-resistant) and KMS28 (bortezomib-sensitive) cell lines were used. 3-[4,5-Dimethylthiazol-2-yl] 1-2,5-diphenylte-trazolium bromide (MTT) assay was performed to determine IC50 values of bortezomib. RNAs were isolated from bortezomib-treated cell lines, followed by cDNA synthesis. Expression levels of the genes were analyzed by using q-Realtime-PCR. Results: As a result, Bcl-2/Bax ratio was higher in KMS20 (resistant) cells than in KMS28 (sensitive) cells. Expression of caspase-3 decreased in KMS20-cells, whereas increased in KMS28-cells. The results indicate that apoptosis was suppressed in resistant cells. Conclusion: These findings will enable us to understand the molecular mechanisms leading to drug-resistance in MM cells and to develop new methods to prevent the resistance. Consequently, preventing the development of bortezomib resistance by eliminating the factors which suppress apoptosis may be a new hope for MM treatment. | |
| dc.identifier.doi | 10.1515/tjb-2019-0521 | |
| dc.identifier.endpage | 69 | en_US |
| dc.identifier.issue | 1 | en_US |
| dc.identifier.scopusquality | Q3 | |
| dc.identifier.startpage | 63 | en_US |
| dc.identifier.uri | https:/dx.doi.org/10.1515/tjb-2019-0521 | |
| dc.identifier.uri | https://hdl.handle.net/20.500.12451/7966 | |
| dc.identifier.volume | 46 | en_US |
| dc.identifier.wos | WOS:000625120300010 | |
| dc.identifier.wosquality | Q4 | |
| dc.indekslendigikaynak | Web of Science | |
| dc.indekslendigikaynak | Scopus | |
| dc.language.iso | en | |
| dc.publisher | Walter de Gruyter | |
| dc.relation.ispartof | Turkish Journal of Biochemistry | |
| dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | Multiple Myeloma | |
| dc.subject | Bortezomib | |
| dc.subject | Drug-Resistance | |
| dc.subject | Apoptosis | |
| dc.subject | BcI-2/Bax | |
| dc.subject | Cancer | |
| dc.title | Inhibition of apoptosis may lead to the development of bortezomib resistance in multiple myeloma cancer cells | |
| dc.type | Article |
