Regulation of Autophagy Is a Novel Tumorigenesis-Related Activity of Multifunctional Translationally Controlled Tumor Protein
Identifieur interne : 000935 ( Pmc/Curation ); précédent : 000934; suivant : 000936Regulation of Autophagy Is a Novel Tumorigenesis-Related Activity of Multifunctional Translationally Controlled Tumor Protein
Auteurs : Ji-Sun Lee ; Eun-Hwa Jang ; Hyun Ae Woo ; Kyunglim LeeSource :
- Cells [ 2073-4409 ] ; 2020.
Abstract
Translationally controlled tumor protein (TCTP) is highly conserved in eukaryotic organisms and plays multiple roles regulating cellular growth and homeostasis. Because of its anti-apoptotic activity and its role in the regulation of cancer metastasis, TCTP has become a promising target for cancer therapy. Moreover, growing evidence points to its clinical role in cancer prognosis. How TCTP regulates cellular growth in cancer has been widely studied, but how it regulates cellular homeostasis has received relatively little attention. This review discusses how TCTP is related to cancer and its potential as a target in cancer therapeutics, including its novel role in the regulation of autophagy. Regulation of autophagy is essential for cell recycling and scavenging cellular materials to sustain cell survival under the metabolic stress that cancer cells undergo during their aggressive proliferation.
Url:
DOI: 10.3390/cells9010257
PubMed: 31968668
PubMed Central: 7017196
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Regulation of Autophagy Is a Novel Tumorigenesis-Related Activity of Multifunctional Translationally Controlled Tumor Protein</title>
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<front><div type="abstract" xml:lang="en"><p>Translationally controlled tumor protein (TCTP) is highly conserved in eukaryotic organisms and plays multiple roles regulating cellular growth and homeostasis. Because of its anti-apoptotic activity and its role in the regulation of cancer metastasis, TCTP has become a promising target for cancer therapy. Moreover, growing evidence points to its clinical role in cancer prognosis. How TCTP regulates cellular growth in cancer has been widely studied, but how it regulates cellular homeostasis has received relatively little attention. This review discusses how TCTP is related to cancer and its potential as a target in cancer therapeutics, including its novel role in the regulation of autophagy. Regulation of autophagy is essential for cell recycling and scavenging cellular materials to sustain cell survival under the metabolic stress that cancer cells undergo during their aggressive proliferation.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cells</journal-id>
<journal-id journal-id-type="iso-abbrev">Cells</journal-id>
<journal-id journal-id-type="publisher-id">cells</journal-id>
<journal-title-group><journal-title>Cells</journal-title>
</journal-title-group>
<issn pub-type="epub">2073-4409</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31968668</article-id>
<article-id pub-id-type="pmc">7017196</article-id>
<article-id pub-id-type="doi">10.3390/cells9010257</article-id>
<article-id pub-id-type="publisher-id">cells-09-00257</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Regulation of Autophagy Is a Novel Tumorigenesis-Related Activity of Multifunctional Translationally Controlled Tumor Protein</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Lee</surname>
<given-names>Ji-Sun</given-names>
</name>
</contrib>
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<given-names>Eun-Hwa</given-names>
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<contrib contrib-type="author"><name><surname>Woo</surname>
<given-names>Hyun Ae</given-names>
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<contrib contrib-type="author"><name><surname>Lee</surname>
<given-names>Kyunglim</given-names>
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<xref rid="c1-cells-09-00257" ref-type="corresp">*</xref>
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</contrib-group>
<aff id="af1-cells-09-00257">Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, Seoul 03760, Korea;<email>leejisun78@hanmail.net</email>
(J.-S.L.);<email>ehj_@naver.com</email>
(E.-H.J.);<email>hawoo@ewha.ac.kr</email>
(H.A.W.)</aff>
<author-notes><corresp id="c1-cells-09-00257"><label>*</label>
Correspondence: <email>klyoon@ewha.ac.kr</email>
; Tel.: +82-2-3277-3024</corresp>
</author-notes>
<pub-date pub-type="epub"><day>20</day>
<month>1</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="collection"><month>1</month>
<year>2020</year>
</pub-date>
<volume>9</volume>
<issue>1</issue>
<elocation-id>257</elocation-id>
<history><date date-type="received"><day>14</day>
<month>11</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>17</day>
<month>1</month>
<year>2020</year>
</date>
</history>
<permissions><copyright-statement>© 2020 by the authors.</copyright-statement>
<copyright-year>2020</copyright-year>
<license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
).</license-p>
</license>
</permissions>
<abstract><p>Translationally controlled tumor protein (TCTP) is highly conserved in eukaryotic organisms and plays multiple roles regulating cellular growth and homeostasis. Because of its anti-apoptotic activity and its role in the regulation of cancer metastasis, TCTP has become a promising target for cancer therapy. Moreover, growing evidence points to its clinical role in cancer prognosis. How TCTP regulates cellular growth in cancer has been widely studied, but how it regulates cellular homeostasis has received relatively little attention. This review discusses how TCTP is related to cancer and its potential as a target in cancer therapeutics, including its novel role in the regulation of autophagy. Regulation of autophagy is essential for cell recycling and scavenging cellular materials to sustain cell survival under the metabolic stress that cancer cells undergo during their aggressive proliferation.</p>
</abstract>
<kwd-group><kwd>TCTP</kwd>
<kwd>cancer</kwd>
<kwd>autophagy</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="cells-09-00257-f001" orientation="portrait" position="float"><label>Figure 1</label>
<caption><p>Negative regulation of autophagy by TCTP. In the initiation step of autophagy, TCTP may inhibit AMPK-induced ULK1 phosphorylation on Ser317 and Ser777, which activates the formation of the Beclin 1 complex. TCTP also enhances the mTORC1-induced phosphorylation of ULK1 on Ser757, which prevents ULK1 interaction with AMPK. TCTP also inhibits autophagosome formation by activating Bcl-2, which, in turn, inhibits the formation of the Beclin1 complex (see text for further details).</p>
</caption>
<graphic xlink:href="cells-09-00257-g001"></graphic>
</fig>
<table-wrap id="cells-09-00257-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">cells-09-00257-t001_Table 1</object-id>
<label>Table 1</label>
<caption><p>Roles of translationally controlled tumor protein (TCTP) in cancer pathogenesis.</p>
</caption>
<table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Function</th>
<th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Mechanism</th>
<th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Reference</th>
</tr>
</thead>
<tbody><tr><td rowspan="4" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Anti-apoptosis</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Increased Mcl-1 stability</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B8-cells-09-00257" ref-type="bibr">8</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inhibition of Bax dimerization</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B9-cells-09-00257" ref-type="bibr">9</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Interaction with ATM and p53</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B11-cells-09-00257" ref-type="bibr">11</xref>
,<xref rid="B12-cells-09-00257" ref-type="bibr">12</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Promotion of MDM2-mediate p53 degradation</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B22-cells-09-00257" ref-type="bibr">22</xref>
]</td>
</tr>
<tr><td rowspan="3" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Pro-metastasis</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cdc42/JNK/MMP9 activation</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B14-cells-09-00257" ref-type="bibr">14</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Regulation of HMGB1/NF-kB activation</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B17-cells-09-00257" ref-type="bibr">17</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Promotion of EMT through mTORC2/Akt/GSK3β/β-catenin pathway</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B15-cells-09-00257" ref-type="bibr">15</xref>
]</td>
</tr>
<tr><td rowspan="3" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Resistance to anti-cancer therapy</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Prevention of apoptosis through association with Apaf-1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B16-cells-09-00257" ref-type="bibr">16</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Translational upregulation of TCTP via mTORC1 pathway</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B21-cells-09-00257" ref-type="bibr">21</xref>
]</td>
</tr>
<tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Promotion of MDM2-mediated p53 degradation</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B24-cells-09-00257" ref-type="bibr">24</xref>
]</td>
</tr>
</tbody>
</table>
</table-wrap>
</floats-group>
</pmc>
</record>
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