Untangling knots between autophagic targets and candidate drugs, in cancer therapy
Identifieur interne : 000F15 ( Main/Exploration ); précédent : 000F14; suivant : 000F16Untangling knots between autophagic targets and candidate drugs, in cancer therapy
Auteurs : Tao Xie [République populaire de Chine] ; Si-Jia Li [République populaire de Chine] ; Ming-Rui Guo [République populaire de Chine] ; Yue Wu [République populaire de Chine] ; Hang-Yu Wang [République populaire de Chine] ; Ke Zhang [République populaire de Chine] ; Xue Zhang [République populaire de Chine] ; Liang Ouyang [République populaire de Chine] ; Jie Liu [République populaire de Chine]Source :
- Cell Proliferation [ 0960-7722 ] ; 2015-04.
Abstract
Autophagy is an evolutionarily conserved lysosomal mechanism implicated in a wide variety of pathological processes, such as cancer. Autophagy can be regulated by a limited number of autophagy‐related genes (Atgs) such as oncogenic Bcl‐2/Bcl‐XL, mTORC1, Akt and PI3KCI, and tumour suppressive proteins PI3KCIII, Beclin‐1, Bif‐1, p53, DAPKs, PTEN and UVRAG, which play their crucial roles in regulating autophagy‐related cancer. As autophagy has a dual role in cancer cells, with tumour‐promoting and tumour‐suppressing properties, it has become an attractive target for a series of emerging small molecule drugs. In this review, we reveal new discoveries of related small molecules or chemical compounds that can regulate autophagic pathways and lead to pro‐death or pro‐survival autophagy, in different types of cancer. We discuss the knots between autophagic targets and candidate drugs, in the hope of shedding new light on exploiting new anti‐tumour small molecule drugs for future cancer therapy.
Url:
DOI: 10.1111/cpr.12167
Affiliations:
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last="Wang">Hang-Yu Wang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Pharmacy, Shihezi University, 832002, Shihezi</wicri:regionArea><wicri:noRegion>Shihezi</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Ke" sort="Zhang, Ke" uniqKey="Zhang K" first="Ke" last="Zhang">Ke Zhang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Pharmacy, Shihezi University, 832002, Shihezi</wicri:regionArea><wicri:noRegion>Shihezi</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Xue" sort="Zhang, Xue" uniqKey="Zhang X" first="Xue" last="Zhang">Xue Zhang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Structure‐Based Drug Design & Discovery of Ministry of Education, School of Traditional Chinese Materia Medica, Shenyang 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Chengdu</wicri:regionArea><wicri:noRegion>Chengdu</wicri:noRegion></affiliation><affiliation></affiliation><affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Cell Proliferation</title><title level="j" type="alt">CELL PROLIFERATION</title><idno type="ISSN">0960-7722</idno><idno type="eISSN">1365-2184</idno><imprint><biblScope unit="vol">48</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="119">119</biblScope><biblScope unit="page" to="139">139</biblScope><biblScope unit="page-count">21</biblScope><date type="published" when="2015-04">2015-04</date></imprint><idno type="ISSN">0960-7722</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0960-7722</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Autophagy is an evolutionarily conserved lysosomal mechanism implicated in a wide variety of pathological processes, such as cancer. Autophagy can be regulated by a limited number of autophagy‐related genes (Atgs) such as oncogenic Bcl‐2/Bcl‐XL, mTORC1, Akt and PI3KCI, and tumour suppressive proteins PI3KCIII, Beclin‐1, Bif‐1, p53, DAPKs, PTEN and UVRAG, which play their crucial roles in regulating autophagy‐related cancer. As autophagy has a dual role in cancer cells, with tumour‐promoting and tumour‐suppressing properties, it has become an attractive target for a series of emerging small molecule drugs. In this review, we reveal new discoveries of related small molecules or chemical compounds that can regulate autophagic pathways and lead to pro‐death or pro‐survival autophagy, in different types of cancer. 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