Shikonin induces colorectal carcinoma cells apoptosis and autophagy by targeting galectin-1/JNK signaling axis
Identifieur interne : 000052 ( Main/Exploration ); précédent : 000051; suivant : 000053Shikonin induces colorectal carcinoma cells apoptosis and autophagy by targeting galectin-1/JNK signaling axis
Auteurs : Nan Zhang [République populaire de Chine] ; Fu Peng [République populaire de Chine] ; Yujia Wang [République populaire de Chine] ; Li Yang [République populaire de Chine] ; Fengbo Wu [République populaire de Chine] ; Xiaoyun Wang [République populaire de Chine] ; Cui Ye [République populaire de Chine] ; Bo Han [République populaire de Chine] ; Gu He [République populaire de Chine]Source :
- International Journal of Biological Sciences [ 1449-2288 ] ; 2020.
Abstract
Colorectal carcinoma (CRC) is the third most common malignant tumor pathology worldwide. Despite progress in surgical procedures and therapy options, CRC is still a considerable cause of cancer-related mortality. In this study, we tested the antitumor effects of shikonin in CRC and tried to identify its potential mechanism. The potential target, molecular mechanism as well as
Url:
DOI: 10.7150/ijbs.36955
PubMed: 31892852
PubMed Central: 6930377
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Colorectal carcinoma (CRC) is the third most common malignant tumor pathology worldwide. Despite progress in surgical procedures and therapy options, CRC is still a considerable cause of cancer-related mortality. In this study, we tested the antitumor effects of shikonin in CRC and tried to identify its potential mechanism. The potential target, molecular mechanism as well as <italic>in vitro</italic>
and <italic>in vivo</italic>
antitumor effects of shikonin in CRC cells were determined by an integrative protocol including quantitative proteomics, RT-PCR, western blotting, RNA interference and overexpression, apoptosis and autophagy assays, etc. Galectin-1 was a potential target of shikonin from the iTRAQ-based proteomic analysis in shikonin-treated SW620 cell. The overexpression and RNA silencing of galectin-1 in two CRC cells suggested that the shikonin sensitivity was correlation to galectin-1 levels. The ROS accumulation induced by shikonin was important to the formation of galectin-1 dimers. Dimer galectin-1 was found to be associated with the activation of JNK and downstream apoptosis or autophagy. Moreover, through functional <italic>in vitro</italic>
studies, we showed that differences in galectin-1 level affected tumor cell proliferation, migration, and invasion. In summary, shikonin induced CRC cells apoptosis and autophagy by targeting galectin-1 and JNK signaling pathway both <italic>in vitro</italic>
and <italic>in vivo</italic>
, which suggested a potential novel therapy target for CRC.</p>
</div>
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</div1>
</back>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Nan" sort="Zhang, Nan" uniqKey="Zhang N" first="Nan" last="Zhang">Nan Zhang</name>
</noRegion>
<name sortKey="Han, Bo" sort="Han, Bo" uniqKey="Han B" first="Bo" last="Han">Bo Han</name>
<name sortKey="He, Gu" sort="He, Gu" uniqKey="He G" first="Gu" last="He">Gu He</name>
<name sortKey="Peng, Fu" sort="Peng, Fu" uniqKey="Peng F" first="Fu" last="Peng">Fu Peng</name>
<name sortKey="Wang, Xiaoyun" sort="Wang, Xiaoyun" uniqKey="Wang X" first="Xiaoyun" last="Wang">Xiaoyun Wang</name>
<name sortKey="Wang, Yujia" sort="Wang, Yujia" uniqKey="Wang Y" first="Yujia" last="Wang">Yujia Wang</name>
<name sortKey="Wu, Fengbo" sort="Wu, Fengbo" uniqKey="Wu F" first="Fengbo" last="Wu">Fengbo Wu</name>
<name sortKey="Yang, Li" sort="Yang, Li" uniqKey="Yang L" first="Li" last="Yang">Li Yang</name>
<name sortKey="Ye, Cui" sort="Ye, Cui" uniqKey="Ye C" first="Cui" last="Ye">Cui Ye</name>
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</tree>
</affiliations>
</record>
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