onr:"swepub:oai:DiVA.org:liu-96160"
Search: onr:"swepub:oai:DiVA.org:liu-96160" > Upregulation of the...
- 1 of 1
- Previous record
- Next record
- To hitlist
- Ding, Zhen-YuLinköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet (author)
Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells
- Article/chapterEnglish2013
Publisher, publication year, extent ...
- 2012-11-28
- Karger / Springer Verlag (Germany),2013
- electronicrdacarrier
Numbers
- LIBRIS-ID:oai:DiVA.org:liu-96160
- https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-96160URI
- https://doi.org/10.1007/s13277-012-0596-8DOI
Supplementary language notes
- Language:English
- Summary in:English
Part of subdatabase
- SwePubSwePub
Classification
Notes
- The antiapoptotic factor Livin has been considered critical for tumor progression and poor prognosis for variant types of tumors. However, there are only limited reports regarding its expression and biological functions in colon cancer. Here, we examined Livin expression in four colon cancer cell lines (HCT116, RKO, KM12C, and SW620) in the presence or absence of cisplatin that was used as a model reagent. We found the different response to cisplatin was related to endogenous Livin expression level. From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was upregulated after cisplatin treatment in a dose-dependent manner. Both immunocytochemistry and nuclear cytoplasmic fractionation indicated Livin remained in the cytoplasm after treatment with cisplatin. In an attempt to explore the mechanism, we found the elevated expression of Livin was not due to the decreased degradation by proteosome but was enhanced at the mRNA level. Besides, cisplatin treatment activated the mammalian target of rapamycin (mTOR) pathway as shown by increased phosphorylation of Akt1, mTOR, S6K, and 4E-BP1, together with the elevated Livin. The PI3K inhibitor LY294002 inhibited both the phosphorylation of mTOR and upregulation of Livin. The stable overexpression of Livin inhibited the activation of caspase-3 and led to resistance to cisplatin, while the knockdown of Livin by siRNA rendered colon cancer cells more sensitive to cisplatin. Our study, along with others, highlighted the potential of Livin for cancer therapy in colon cancer.
Subject headings and genre
- Livin; Apoptosis; Cisplatin; Colon cancer
- MEDICINE
- MEDICIN
Added entries (persons, corporate bodies, meetings, titles ...)
- Liu, Gui-HongSichuan University, China (author)
- Olsson, BirgitLinköpings universitet,Onkologi,Hälsouniversitetet(Swepub:liu)birol93 (author)
- Sun, Xiao-FengÖstergötlands Läns Landsting,Linköpings universitet,Avdelningen för kliniska vetenskaper,Hälsouniversitetet,Onkologiska kliniken US(Swepub:liu)xiasu45 (author)
- Linköpings universitetInstitutionen för klinisk och experimentell medicin (creator_code:org_t)
Related titles
- In:Tumor Biology: Karger / Springer Verlag (Germany)34:2, s. 683-6931010-42831423-0380
Internet link
Find in a library
- Tumor Biology (Search for host publication in LIBRIS)
To the university's database
- 1 of 1
- Previous record
- Next record
- To hitlist
Find more in SwePub
- By the author/editor
- Ding, Zhen-Yu
- Liu, Gui-Hong
- Olsson, Birgit
- Sun, Xiao-Feng
- Articles in the publication
- Tumor Biology
- By the university
- Linköping University
Search outside SwePub
- Extend your search to:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - National Library Systems
- LIBRIS.kb.se
