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פותח על ידי קלירמאש פתרונות בע"מ -
The characterization of the effects of the strigolactones on the heat shock response [abstract]
Year:
2015
Source of publication :
Cancer Research
Authors :
קולטאי, חננית
;
.
קפולניק, יורם
;
.
Volume :
75 (suppl. 15)
Co-Authors:

Victor S. Wang, Nu Nu Kyin, Claire Pollock, Hyjoung Lee, Xin Li, Cristina Prandi, Luke Whitesell, Ronit Yarden

Facilitators :
From page:
0
To page:
0
(
Total pages:
1
)
Abstract:

Strigolactones (SLs) are a novel class of plant hormones that inhibit the self-renewal of undifferentiated meristem cells in shoots regulating above-ground plant architecture. Data from our lab have shown that SL analogues are able to inhibit the growth and survival of a wide array of cancer-derived cell lines including: prostate, colon, lung, breast and osteosarcoma (U2OS) while minimally affecting cultured normal cells. Treatment of cancer cells with SL analogues leads to the activation of stress-related signaling including p38MAPKs and JNK1/2, as well as the activation of the heat shock master regulator, heat shock transcription factor 1 (HSF1), and heat shock response (HSR) gene expression. We further show that SLs generate reactive oxygen species (ROS) and that SL treatments of cancer cells leads to the activation of GRP78, the master regulator of the unfolded protein response (UPR). To further characterize the relationship between SLs, HSR and UPR, several clones of HSF1 shRNA knockdown, in U2OS cells were generated and are currently being studied. Interestingly, while wild type mouse embryonic fibroblast (MEF) cells are refractory to SLs treatments, we demonstrate that HSF1 knockout in MEFs enhances the sensitivity of the cells to SLs treatments. Taken together, our data suggest that the HSR and UPR are recruited as cell survival mechanisms against the SLs treatments, giving rise to possible future chemotherapeutic combinatorial treatment options.

Note:

Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA.

Abstract no. 1777

 

Related Files :
Cancer
cancer (disease)
heat shock
plant hormones
Strigolactones
עוד תגיות
תוכן קשור
More details
DOI :
doi:10.1158/1538-7445.AM2015-1777
Article number:
1777
Affiliations:
Database:
גוגל סקולר
Publication Type:
מאמר מתוך כינוס
;
.
תקציר
;
.
Language:
אנגלית
Editors' remarks:
ID:
39151
Last updated date:
02/03/2022 17:27
Creation date:
30/01/2019 12:23
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Scientific Publication
The characterization of the effects of the strigolactones on the heat shock response [abstract]
75 (suppl. 15)

Victor S. Wang, Nu Nu Kyin, Claire Pollock, Hyjoung Lee, Xin Li, Cristina Prandi, Luke Whitesell, Ronit Yarden

The characterization of the effects of the strigolactones on the heat shock response

Strigolactones (SLs) are a novel class of plant hormones that inhibit the self-renewal of undifferentiated meristem cells in shoots regulating above-ground plant architecture. Data from our lab have shown that SL analogues are able to inhibit the growth and survival of a wide array of cancer-derived cell lines including: prostate, colon, lung, breast and osteosarcoma (U2OS) while minimally affecting cultured normal cells. Treatment of cancer cells with SL analogues leads to the activation of stress-related signaling including p38MAPKs and JNK1/2, as well as the activation of the heat shock master regulator, heat shock transcription factor 1 (HSF1), and heat shock response (HSR) gene expression. We further show that SLs generate reactive oxygen species (ROS) and that SL treatments of cancer cells leads to the activation of GRP78, the master regulator of the unfolded protein response (UPR). To further characterize the relationship between SLs, HSR and UPR, several clones of HSF1 shRNA knockdown, in U2OS cells were generated and are currently being studied. Interestingly, while wild type mouse embryonic fibroblast (MEF) cells are refractory to SLs treatments, we demonstrate that HSF1 knockout in MEFs enhances the sensitivity of the cells to SLs treatments. Taken together, our data suggest that the HSR and UPR are recruited as cell survival mechanisms against the SLs treatments, giving rise to possible future chemotherapeutic combinatorial treatment options.

Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA.

Abstract no. 1777

 

Scientific Publication
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