Cargando…

Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance

As the major and preferred treatment for ovarian cancer ascites, chemotherapy can reduce or inhibit recurrent ascites (hereafter re-ascites); however, some patients still experience re-ascites. Therefore, this study investigated cases in which epithelial ovarian cancer (EOC) patients experienced re-...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Yu, Tang, Jing, Liu, Duanyang, Zhang, Lei, He, Yan, Li, Jing, Gao, Lei, Tang, Dai, Jin, Xiaoming, Kong, Dan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5856849/
https://www.ncbi.nlm.nih.gov/pubmed/29549251
http://dx.doi.org/10.1038/s41419-018-0449-5
_version_ 1783307354281869312
author Liu, Yu
Tang, Jing
Liu, Duanyang
Zhang, Lei
He, Yan
Li, Jing
Gao, Lei
Tang, Dai
Jin, Xiaoming
Kong, Dan
author_facet Liu, Yu
Tang, Jing
Liu, Duanyang
Zhang, Lei
He, Yan
Li, Jing
Gao, Lei
Tang, Dai
Jin, Xiaoming
Kong, Dan
author_sort Liu, Yu
collection PubMed
description As the major and preferred treatment for ovarian cancer ascites, chemotherapy can reduce or inhibit recurrent ascites (hereafter re-ascites); however, some patients still experience re-ascites. Therefore, this study investigated cases in which epithelial ovarian cancer (EOC) patients experienced re-ascites. In re-ascites cases, CA125, MDR1, LC-3, and Beclin-1 were highly expressed. In addition, CASP-9 and c-CASP-3 expression levels were decreased, and serum CA125 levels (highest 4348 U/ml) were increased compared to chemosensitive cases. The results suggest that high expression levels of Beclin-1 and LC-3, thus increasing the level of autophagy and inhibiting apoptosis in the no-chemotherapy group. In the chemosensitive group, survivin expression was decreased and CASP-9 expression was increased, which led to c-CASP-3 activation and increased tumor cell apoptosis. The results of the cell lines confirm that inhibition of autophagy can increase the sensitivity of ovarian cancer cells to CDDP and promote CDDP-induced cell death. Re-ascites, which appears after chemotherapy, may be associated with drug resistance. In addition, increased autophagy may protect tumor cells from chemotherapeutic drugs, thus inhibiting tumor cell death.
format Online
Article
Text
id pubmed-5856849
institution National Center for Biotechnology Information
language English
publishDate 2018
publisher Nature Publishing Group UK
record_format MEDLINE/PubMed
spelling pubmed-58568492018-06-04 Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance Liu, Yu Tang, Jing Liu, Duanyang Zhang, Lei He, Yan Li, Jing Gao, Lei Tang, Dai Jin, Xiaoming Kong, Dan Cell Death Dis Article As the major and preferred treatment for ovarian cancer ascites, chemotherapy can reduce or inhibit recurrent ascites (hereafter re-ascites); however, some patients still experience re-ascites. Therefore, this study investigated cases in which epithelial ovarian cancer (EOC) patients experienced re-ascites. In re-ascites cases, CA125, MDR1, LC-3, and Beclin-1 were highly expressed. In addition, CASP-9 and c-CASP-3 expression levels were decreased, and serum CA125 levels (highest 4348 U/ml) were increased compared to chemosensitive cases. The results suggest that high expression levels of Beclin-1 and LC-3, thus increasing the level of autophagy and inhibiting apoptosis in the no-chemotherapy group. In the chemosensitive group, survivin expression was decreased and CASP-9 expression was increased, which led to c-CASP-3 activation and increased tumor cell apoptosis. The results of the cell lines confirm that inhibition of autophagy can increase the sensitivity of ovarian cancer cells to CDDP and promote CDDP-induced cell death. Re-ascites, which appears after chemotherapy, may be associated with drug resistance. In addition, increased autophagy may protect tumor cells from chemotherapeutic drugs, thus inhibiting tumor cell death. Nature Publishing Group UK 2018-03-16 /pmc/articles/PMC5856849/ /pubmed/29549251 http://dx.doi.org/10.1038/s41419-018-0449-5 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Liu, Yu
Tang, Jing
Liu, Duanyang
Zhang, Lei
He, Yan
Li, Jing
Gao, Lei
Tang, Dai
Jin, Xiaoming
Kong, Dan
Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance
title Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance
title_full Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance
title_fullStr Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance
title_full_unstemmed Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance
title_short Increased autophagy in EOC re-ascites cells can inhibit cell death and promote drug resistance
title_sort increased autophagy in eoc re-ascites cells can inhibit cell death and promote drug resistance
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5856849/
https://www.ncbi.nlm.nih.gov/pubmed/29549251
http://dx.doi.org/10.1038/s41419-018-0449-5
work_keys_str_mv AT liuyu increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT tangjing increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT liuduanyang increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT zhanglei increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT heyan increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT lijing increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT gaolei increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT tangdai increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT jinxiaoming increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance
AT kongdan increasedautophagyineocreascitescellscaninhibitcelldeathandpromotedrugresistance