ROLE OF Wip1-p53 AXIS IN RESPONSE OF MURINE CELLS TO TREATMENT WITH SODIUM BUTYRATE AND MEK/ERK SIGNALLING PATHWAY INHIBITOR
The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes inv...
Uloženo v:
| Vydáno v: | T͡S︡itologii͡a Ročník 59; číslo 4; s. 285 |
|---|---|
| Hlavní autoři: | , |
| Médium: | Journal Article |
| Jazyk: | angličtina ruština |
| Vydáno: |
Russia (Federation)
2017
|
| ISSN: | 0041-3771 |
| On-line přístup: | Zjistit podrobnosti o přístupu |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes involved in anti-cancer therapy response, Wip1 phosphatase and p53. We have investigated the effect of these agents on cell cycle of wild-type cells, Wip1 knockout cells and cells with double deletion of Wip1 and p53. Our results showed that more severe changes in S and G2/M phases were observed in response to sodium butyrate in Wip1-defecient cells than in wild-type cells. Meanwhile, PD0325901 treatment led to G1 arrest. At the same time, a «sodium butyrate type» response dominated the response to combined treatment with both drugs in Wip1-deficient cells, while the response of Wip1–/–/p53–/– cells to combined treatment was similar to the single use of PD0325901. Wip1–/– and Wip1–/–/p53–/– cells were more sensitive to the use of PD0325901 than wild-type cells. Obtained results suggest that Wip1 deficiency sensitizes cells to sodium butyrate and to MEK/ERK inhibitors independently from Wip1 main target protein — p53. Data acquired give insights into role of Wip1 in cellular responses to treatment with HDAC and MEK/ERK inhibitors. |
|---|---|
| AbstractList | The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes involved in anti-cancer therapy response, Wip1 phosphatase and p53. We have investigated the effect of these agents on cell cycle of wild-type cells, Wip1 knockout cells and cells with double deletion of Wip1 and p53. Our results showed that more severe changes in S and G2/M phases were observed in response to sodium butyrate in Wip1-defecient cells than in wild-type cells. Meanwhile, PD0325901 treatment led to G1 arrest. At the same time, a «sodium butyrate type» response dominated the response to combined treatment with both drugs in Wip1-deficient cells, while the response of Wip1–/–/p53–/– cells to combined treatment was similar to the single use of PD0325901. Wip1–/– and Wip1–/–/p53–/– cells were more sensitive to the use of PD0325901 than wild-type cells. Obtained results suggest that Wip1 deficiency sensitizes cells to sodium butyrate and to MEK/ERK inhibitors independently from Wip1 main target protein — p53. Data acquired give insights into role of Wip1 in cellular responses to treatment with HDAC and MEK/ERK inhibitors.The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes involved in anti-cancer therapy response, Wip1 phosphatase and p53. We have investigated the effect of these agents on cell cycle of wild-type cells, Wip1 knockout cells and cells with double deletion of Wip1 and p53. Our results showed that more severe changes in S and G2/M phases were observed in response to sodium butyrate in Wip1-defecient cells than in wild-type cells. Meanwhile, PD0325901 treatment led to G1 arrest. At the same time, a «sodium butyrate type» response dominated the response to combined treatment with both drugs in Wip1-deficient cells, while the response of Wip1–/–/p53–/– cells to combined treatment was similar to the single use of PD0325901. Wip1–/– and Wip1–/–/p53–/– cells were more sensitive to the use of PD0325901 than wild-type cells. Obtained results suggest that Wip1 deficiency sensitizes cells to sodium butyrate and to MEK/ERK inhibitors independently from Wip1 main target protein — p53. Data acquired give insights into role of Wip1 in cellular responses to treatment with HDAC and MEK/ERK inhibitors. The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes involved in anti-cancer therapy response, Wip1 phosphatase and p53. We have investigated the effect of these agents on cell cycle of wild-type cells, Wip1 knockout cells and cells with double deletion of Wip1 and p53. Our results showed that more severe changes in S and G2/M phases were observed in response to sodium butyrate in Wip1-defecient cells than in wild-type cells. Meanwhile, PD0325901 treatment led to G1 arrest. At the same time, a «sodium butyrate type» response dominated the response to combined treatment with both drugs in Wip1-deficient cells, while the response of Wip1–/–/p53–/– cells to combined treatment was similar to the single use of PD0325901. Wip1–/– and Wip1–/–/p53–/– cells were more sensitive to the use of PD0325901 than wild-type cells. Obtained results suggest that Wip1 deficiency sensitizes cells to sodium butyrate and to MEK/ERK inhibitors independently from Wip1 main target protein — p53. Data acquired give insights into role of Wip1 in cellular responses to treatment with HDAC and MEK/ERK inhibitors. |
| Author | Kochetkova, E ayu Demidov, O N |
| Author_xml | – sequence: 1 givenname: E ayu surname: Kochetkova fullname: Kochetkova, E ayu – sequence: 2 givenname: O N surname: Demidov fullname: Demidov, O N |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30188093$$D View this record in MEDLINE/PubMed |
| BookMark | eNo1kDtvwjAYRT1QFUr5C5XHLlE_x3GcjAYMscgDJUaUKQq2I1HxKilDpf74oj6mO9yjo6v7gHrH09H10AAgIB7lnPTRqOveAIAADVjE71GfAokiiOkAfZVFKnExw-vdmXhnRrF4VRVWOS5ltSzy6qfMVqXKJZ7INK2wLrAupdCZzDVeK53gqpiqVYbHK70phZZY5FOcycWLLBe4UvNcpKnK53gpdLIWm5s8UWOli_IR3bXNvnOjvxwiPZN6knhpMVcTkd72hNQzrW0JM03DQ8usdVsGcUwaG8LWGMNtzGLGI0PayEUu9CmEnJnQcg5BCDaO_CF6_tWeL6f3q-s-6sOuM26_b47udO1qnwBQnwfg39CnP_S6PThbny-7Q3P5rP8P878BBQNeJQ |
| ContentType | Journal Article |
| DBID | NPM 7X8 |
| DatabaseName | PubMed MEDLINE - Academic |
| DatabaseTitle | PubMed MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic PubMed |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | no_fulltext_linktorsrc |
| Discipline | Biology |
| ExternalDocumentID | 30188093 |
| Genre | Journal Article English Abstract |
| GroupedDBID | ALMA_UNASSIGNED_HOLDINGS F5P NPM RUPBI SV3 VCL VIT 7X8 |
| ID | FETCH-LOGICAL-p563-cfdf15caa76d5ddeb50991ad60bccc7d959578c1f8e8e6230675c6d770460d982 |
| IEDL.DBID | 7X8 |
| ISSN | 0041-3771 |
| IngestDate | Thu Oct 02 12:04:25 EDT 2025 Wed Feb 19 02:42:00 EST 2025 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 4 |
| Language | English Russian |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-p563-cfdf15caa76d5ddeb50991ad60bccc7d959578c1f8e8e6230675c6d770460d982 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| PMID | 30188093 |
| PQID | 2100327402 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_2100327402 pubmed_primary_30188093 |
| PublicationCentury | 2000 |
| PublicationDate | 2017 20170101 |
| PublicationDateYYYYMMDD | 2017-01-01 |
| PublicationDate_xml | – year: 2017 text: 2017 |
| PublicationDecade | 2010 |
| PublicationPlace | Russia (Federation) |
| PublicationPlace_xml | – name: Russia (Federation) |
| PublicationTitle | T͡S︡itologii͡a |
| PublicationTitleAlternate | Tsitologiia |
| PublicationYear | 2017 |
| SSID | ssj0001034587 |
| Score | 2.014307 |
| Snippet | The use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | 285 |
| Title | ROLE OF Wip1-p53 AXIS IN RESPONSE OF MURINE CELLS TO TREATMENT WITH SODIUM BUTYRATE AND MEK/ERK SIGNALLING PATHWAY INHIBITOR |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/30188093 https://www.proquest.com/docview/2100327402 |
| Volume | 59 |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1La-MwEBbsZhf2su9H98Us7NXUtmzJOhW3dRpRRw62QtJTiCUbekmyTVso9Md3ZLv0tLCwF1-EbTGa-eYl5iPkNwsb9BqUepYJ6kXWjbyNIu5hOtT4rk0VU9ORTXClkuVSzIaC2364VvmIiR1Q261xNfJDTE18iimUHx7t_niONcp1VwcKjWdkRDGUcVrNl8lTjcWnUZz0YzOjAG2JB38PJDuHMn7zv1t5S14PoSSk_dm_I6NmA1c378nLnl_y7gO5L4s8g2IMi8td4O1iCulSViAVoNxnhaq6xem8lCqDkyzPK9AF6DJLtZvxDwupJ1AVp3I-heO5vihTnUGqTmGanR9m5TlU8kyleS7VGcxSPVmkF_jxiTyWuig_Ej3O9MnEG-gW8P-Meqa1bRCb9ZozGyPo1RhKiGBtmV8bY7gVsUDrNkGbNEnDwi7VMMxy7lqrViThJ_J8s900XwiwoOYxa4WImjBCRK0pp5aKoEa1MJQlB-TXo2BXqM2uRbHeNNub_epJtAfkc386q10_dmOFUIRgI-jXf3j7G3kVOv_b1Uq-k1GLttz8IC_M7fXl_upnpyb4VLPpA9TfvV4 |
| linkProvider | ProQuest |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=ROLE+OF+Wip1-p53+AXIS+IN+RESPONSE+OF+MURINE+CELLS+TO+TREATMENT+WITH+SODIUM+BUTYRATE+AND+MEK%2FERK+SIGNALLING+PATHWAY+INHIBITOR&rft.jtitle=T%CD%A1S%EF%B8%A1itologii%CD%A1a&rft.au=Kochetkova%2C+E+ayu&rft.au=Demidov%2C+O+N&rft.date=2017-01-01&rft.issn=0041-3771&rft.volume=59&rft.issue=4&rft.spage=285&rft_id=info%3Apmid%2F30188093&rft_id=info%3Apmid%2F30188093&rft.externalDocID=30188093 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0041-3771&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0041-3771&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0041-3771&client=summon |