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Knockdown of neuron-specific enolase suppresses the proliferation and migration of NCI-H209 cells

Identifieur interne : 000701 ( Main/Exploration ); précédent : 000700; suivant : 000702

Knockdown of neuron-specific enolase suppresses the proliferation and migration of NCI-H209 cells

Auteurs : Xia Liu [République populaire de Chine] ; Shousheng Liu [République populaire de Chine] ; Juan Fu [République populaire de Chine] ; Jinsheng Huang [République populaire de Chine] ; Chengyin Weng [République populaire de Chine] ; Xisheng Fang [République populaire de Chine] ; Mingmei Guan [République populaire de Chine] ; Yong Wu [République populaire de Chine] ; Lin Yang [République populaire de Chine] ; Guolong Liu [République populaire de Chine]

Source :

RBID : PMC:6781773

Abstract

Neuron-specific enolase (NSE) is generally considered as a marker for diagnosis and evaluation of the response to therapy in small cell lung cancer (SCLC). However, the role of NSE in the progression of SCLC remains to be elucidated. In the present study, the functions of NSE in SCLC, in addition to the potential mechanisms, were investigated using a loss-of-function approach with NSE-targeting small interfering (si)RNA. The knockdown of NSE markedly decreased the proliferation of NCI-H209 cells, as indicated by MTT assay (P<0.05). Furthermore, the silencing of NSE resulted in the formation of smaller and fewer colonies compared with that in the control group (P<0.001). Flow cytometric analysis indicated that the silencing of NSE resulted in a decreased S-phase population among NCI-H209 cells (P<0.05). Transwell assay demonstrated that the silencing of NSE suppressed the migration of NCI-H209 cells (P<0.001). NCI-H209 cells transfected with NSE siRNA-1 or negative control were collected and the protein levels of metastasis-associated genes were detected using western blot analysis. The results indicated that the knockdown of NSE led to downregulation of the pro-metastatic gene vascular endothelial growth factor (VEGF; P<0.05) and the upregulation of metastasis suppressor genes NM23 and E-cadherin (P<0.05). Taken together, the results of the present study demonstrated that the silencing of NSE suppressed the migration, proliferation and colony formation ability of SCLC cells and decreased the S-phase population. In addition, the knockdown of NSE resulted in the upregulation of E-cadherin and NM23 and the downregulation of VEGF. Collectively, these results indicated that intracellular NSE may have an important role in the progression of SCLC.


Url:
DOI: 10.3892/ol.2019.10797
PubMed: 31611991
PubMed Central: 6781773


Affiliations:


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Le document en format XML

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<p>Neuron-specific enolase (NSE) is generally considered as a marker for diagnosis and evaluation of the response to therapy in small cell lung cancer (SCLC). However, the role of NSE in the progression of SCLC remains to be elucidated. In the present study, the functions of NSE in SCLC, in addition to the potential mechanisms, were investigated using a loss-of-function approach with NSE-targeting small interfering (si)RNA. The knockdown of NSE markedly decreased the proliferation of NCI-H209 cells, as indicated by MTT assay (P<0.05). Furthermore, the silencing of NSE resulted in the formation of smaller and fewer colonies compared with that in the control group (P<0.001). Flow cytometric analysis indicated that the silencing of NSE resulted in a decreased S-phase population among NCI-H209 cells (P<0.05). Transwell assay demonstrated that the silencing of NSE suppressed the migration of NCI-H209 cells (P<0.001). NCI-H209 cells transfected with NSE siRNA-1 or negative control were collected and the protein levels of metastasis-associated genes were detected using western blot analysis. The results indicated that the knockdown of NSE led to downregulation of the pro-metastatic gene vascular endothelial growth factor (VEGF; P<0.05) and the upregulation of metastasis suppressor genes NM23 and E-cadherin (P<0.05). Taken together, the results of the present study demonstrated that the silencing of NSE suppressed the migration, proliferation and colony formation ability of SCLC cells and decreased the S-phase population. In addition, the knockdown of NSE resulted in the upregulation of E-cadherin and NM23 and the downregulation of VEGF. Collectively, these results indicated that intracellular NSE may have an important role in the progression of SCLC.</p>
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<name sortKey="Attanasio, C" uniqKey="Attanasio C">C Attanasio</name>
</author>
<author>
<name sortKey="Damiani, V" uniqKey="Damiani V">V Damiani</name>
</author>
<author>
<name sortKey="Boffa, I" uniqKey="Boffa I">I Boffa</name>
</author>
<author>
<name sortKey="Aiese, N" uniqKey="Aiese N">N Aiese</name>
</author>
<author>
<name sortKey="Pedone, E" uniqKey="Pedone E">E Pedone</name>
</author>
<author>
<name sortKey="Accordi, B" uniqKey="Accordi B">B Accordi</name>
</author>
<author>
<name sortKey="Basso, G" uniqKey="Basso G">G Basso</name>
</author>
</analytic>
</biblStruct>
<biblStruct>
<analytic>
<author>
<name sortKey="Esposito, S" uniqKey="Esposito S">S Esposito</name>
</author>
<author>
<name sortKey="Russo, Mv" uniqKey="Russo M">MV Russo</name>
</author>
<author>
<name sortKey="Airoldi, I" uniqKey="Airoldi I">I Airoldi</name>
</author>
<author>
<name sortKey="Tupone, Mg" uniqKey="Tupone M">MG Tupone</name>
</author>
<author>
<name sortKey="Sorrentino, C" uniqKey="Sorrentino C">C Sorrentino</name>
</author>
<author>
<name sortKey="Barbarito, G" uniqKey="Barbarito G">G Barbarito</name>
</author>
<author>
<name sortKey="Di Meo, S" uniqKey="Di Meo S">S Di Meo</name>
</author>
<author>
<name sortKey="Di Carlo, E" uniqKey="Di Carlo E">E Di Carlo</name>
</author>
</analytic>
</biblStruct>
<biblStruct>
<analytic>
<author>
<name sortKey="Huang, Cs" uniqKey="Huang C">CS Huang</name>
</author>
<author>
<name sortKey="Shih, Mk" uniqKey="Shih M">MK Shih</name>
</author>
<author>
<name sortKey="Chuang, Ch" uniqKey="Chuang C">CH Chuang</name>
</author>
<author>
<name sortKey="Hu, Ml" uniqKey="Hu M">ML Hu</name>
</author>
</analytic>
</biblStruct>
<biblStruct>
<analytic>
<author>
<name sortKey="Kim, Yi" uniqKey="Kim Y">YI Kim</name>
</author>
<author>
<name sortKey="Park, S" uniqKey="Park S">S Park</name>
</author>
<author>
<name sortKey="Jeoung, Di" uniqKey="Jeoung D">DI Jeoung</name>
</author>
<author>
<name sortKey="Lee, H" uniqKey="Lee H">H Lee</name>
</author>
</analytic>
</biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Liu, Xia" sort="Liu, Xia" uniqKey="Liu X" first="Xia" last="Liu">Xia Liu</name>
</noRegion>
<name sortKey="Fang, Xisheng" sort="Fang, Xisheng" uniqKey="Fang X" first="Xisheng" last="Fang">Xisheng Fang</name>
<name sortKey="Fu, Juan" sort="Fu, Juan" uniqKey="Fu J" first="Juan" last="Fu">Juan Fu</name>
<name sortKey="Fu, Juan" sort="Fu, Juan" uniqKey="Fu J" first="Juan" last="Fu">Juan Fu</name>
<name sortKey="Guan, Mingmei" sort="Guan, Mingmei" uniqKey="Guan M" first="Mingmei" last="Guan">Mingmei Guan</name>
<name sortKey="Huang, Jinsheng" sort="Huang, Jinsheng" uniqKey="Huang J" first="Jinsheng" last="Huang">Jinsheng Huang</name>
<name sortKey="Huang, Jinsheng" sort="Huang, Jinsheng" uniqKey="Huang J" first="Jinsheng" last="Huang">Jinsheng Huang</name>
<name sortKey="Liu, Guolong" sort="Liu, Guolong" uniqKey="Liu G" first="Guolong" last="Liu">Guolong Liu</name>
<name sortKey="Liu, Shousheng" sort="Liu, Shousheng" uniqKey="Liu S" first="Shousheng" last="Liu">Shousheng Liu</name>
<name sortKey="Liu, Shousheng" sort="Liu, Shousheng" uniqKey="Liu S" first="Shousheng" last="Liu">Shousheng Liu</name>
<name sortKey="Weng, Chengyin" sort="Weng, Chengyin" uniqKey="Weng C" first="Chengyin" last="Weng">Chengyin Weng</name>
<name sortKey="Wu, Yong" sort="Wu, Yong" uniqKey="Wu Y" first="Yong" last="Wu">Yong Wu</name>
<name sortKey="Yang, Lin" sort="Yang, Lin" uniqKey="Yang L" first="Lin" last="Yang">Lin Yang</name>
</country>
</tree>
</affiliations>
</record>

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