Insufficient radiofrequency ablation-induced autophagy contributes to the rapid progression of residual hepatocellular carcinoma through the HIF-1α/BNIP3 signaling pathway
Identifieur interne : 000719 ( Main/Exploration ); précédent : 000718; suivant : 000720Insufficient radiofrequency ablation-induced autophagy contributes to the rapid progression of residual hepatocellular carcinoma through the HIF-1α/BNIP3 signaling pathway
Auteurs : Wen-Lei Xu ; Shao-Hong Wang ; Wen-Bing Sun ; Jun Gao ; Xue-Mei Ding ; Jian Kong ; Li Xu ; Shan KeSource :
- BMB Reports [ 1976-6696 ] ; 2019.
Abstract
Currently speaking, it is noted that radiofrequency ablation (RFA) has been the most widely used treatment for hepatocellular carcinoma (HCC) occurring in patients. However, accumulating evidence has demonstrated that the incidence of insufficient RFA (IRFA) may result in the identified rapid progression of residual HCC in the patient, which can greatly hinder the effectiveness and patient reported benefits of utilizing this technique. Although many efforts have been proposed, the underlying mechanisms triggering the rapid progression of residual HCC after IRFA have not yet been fully clarified through current research literature reviews. It was shown in this study that cell proliferation, migration and invasion of residual HepG2 and SMMC7721 cells were significantly increased after the IRFA was simulated
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DOI: 10.5483/BMBRep.2019.52.4.263
PubMed: 30940322
PubMed Central: 6507849
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Insufficient radiofrequency ablation-induced autophagy contributes to the rapid progression of residual hepatocellular carcinoma through the HIF-1α/BNIP3 signaling pathway</title><author><name sortKey="Xu, Wen Lei" sort="Xu, Wen Lei" uniqKey="Xu W" first="Wen-Lei" last="Xu">Wen-Lei Xu</name></author><author><name sortKey="Wang, Shao Hong" sort="Wang, Shao Hong" uniqKey="Wang S" first="Shao-Hong" last="Wang">Shao-Hong Wang</name></author><author><name sortKey="Sun, Wen Bing" sort="Sun, Wen Bing" uniqKey="Sun W" first="Wen-Bing" last="Sun">Wen-Bing Sun</name></author><author><name sortKey="Gao, Jun" sort="Gao, Jun" uniqKey="Gao J" first="Jun" last="Gao">Jun Gao</name></author><author><name sortKey="Ding, Xue Mei" sort="Ding, Xue Mei" uniqKey="Ding X" first="Xue-Mei" last="Ding">Xue-Mei Ding</name></author><author><name sortKey="Kong, Jian" sort="Kong, Jian" uniqKey="Kong J" first="Jian" last="Kong">Jian Kong</name></author><author><name sortKey="Xu, Li" sort="Xu, Li" uniqKey="Xu L" first="Li" last="Xu">Li Xu</name></author><author><name sortKey="Ke, Shan" sort="Ke, Shan" uniqKey="Ke S" first="Shan" last="Ke">Shan Ke</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30940322</idno><idno type="pmc">6507849</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6507849</idno><idno type="RBID">PMC:6507849</idno><idno type="doi">10.5483/BMBRep.2019.52.4.263</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000415</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000415</idno><idno type="wicri:Area/Pmc/Curation">000415</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000415</idno><idno type="wicri:Area/Pmc/Checkpoint">000665</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000665</idno><idno type="wicri:Area/Ncbi/Merge">000514</idno><idno type="wicri:Area/Ncbi/Curation">000514</idno><idno type="wicri:Area/Ncbi/Checkpoint">000514</idno><idno type="wicri:doubleKey">1976-6696:2019:Xu W:insufficient:radiofrequency:ablation</idno><idno type="wicri:Area/Main/Merge">000719</idno><idno type="wicri:Area/Main/Curation">000719</idno><idno type="wicri:Area/Main/Exploration">000719</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Insufficient radiofrequency ablation-induced autophagy contributes to the rapid progression of residual hepatocellular carcinoma through the HIF-1α/BNIP3 signaling pathway</title><author><name sortKey="Xu, Wen Lei" sort="Xu, Wen Lei" uniqKey="Xu W" first="Wen-Lei" last="Xu">Wen-Lei Xu</name></author><author><name sortKey="Wang, Shao Hong" sort="Wang, Shao Hong" uniqKey="Wang S" first="Shao-Hong" last="Wang">Shao-Hong Wang</name></author><author><name sortKey="Sun, Wen Bing" sort="Sun, Wen Bing" uniqKey="Sun W" first="Wen-Bing" last="Sun">Wen-Bing Sun</name></author><author><name sortKey="Gao, Jun" sort="Gao, Jun" uniqKey="Gao J" first="Jun" last="Gao">Jun Gao</name></author><author><name sortKey="Ding, Xue Mei" sort="Ding, Xue Mei" uniqKey="Ding X" first="Xue-Mei" last="Ding">Xue-Mei Ding</name></author><author><name sortKey="Kong, Jian" sort="Kong, Jian" uniqKey="Kong J" first="Jian" last="Kong">Jian Kong</name></author><author><name sortKey="Xu, Li" sort="Xu, Li" uniqKey="Xu L" first="Li" last="Xu">Li Xu</name></author><author><name sortKey="Ke, Shan" sort="Ke, Shan" uniqKey="Ke S" first="Shan" last="Ke">Shan Ke</name></author></analytic><series><title level="j">BMB Reports</title><idno type="ISSN">1976-6696</idno><idno type="eISSN">1976-670X</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Currently speaking, it is noted that radiofrequency ablation (RFA) has been the most widely used treatment for hepatocellular carcinoma (HCC) occurring in patients. However, accumulating evidence has demonstrated that the incidence of insufficient RFA (IRFA) may result in the identified rapid progression of residual HCC in the patient, which can greatly hinder the effectiveness and patient reported benefits of utilizing this technique. Although many efforts have been proposed, the underlying mechanisms triggering the rapid progression of residual HCC after IRFA have not yet been fully clarified through current research literature reviews. It was shown in this study that cell proliferation, migration and invasion of residual HepG2 and SMMC7721 cells were significantly increased after the IRFA was simulated <italic>in vitro</italic>. In other words, it is noted that IRFA could do this by enhancing the image of autophagy of the residual HCC cell via the HIF-1α/BNIP3 pathway. Consequently, the down-regulation of BNIP3 may result in the inhibition of the residual HCC cell progression and autophagy after IRFA. Our present study results suggest that IRFA could promote residual HCC cell progression <italic>in vitro</italic> by enhancing autophagy via the HIF-1α/BNIP3 pathway. For this reason, it is noted that the targeting of the BNIP3 may be useful in preventing the rapid growth and metastasis of residual HCC after IRFA.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Tang, A" uniqKey="Tang A">A Tang</name></author><author><name sortKey="Hallouch, O" uniqKey="Hallouch O">O Hallouch</name></author><author><name sortKey="Chernyak, V" uniqKey="Chernyak V">V Chernyak</name></author><author><name sortKey="Kamaya, A" uniqKey="Kamaya A">A Kamaya</name></author><author><name sortKey="Sirlin, Cb" uniqKey="Sirlin C">CB Sirlin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Daher, S" uniqKey="Daher S">S Daher</name></author><author><name sortKey="Massarwa, M" uniqKey="Massarwa M">M Massarwa</name></author><author><name sortKey="Benson, Aa" uniqKey="Benson A">AA Benson</name></author><author><name sortKey="Khoury, T" uniqKey="Khoury T">T 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Hoffman</name></author><author><name sortKey="Shanmughapriya, S" uniqKey="Shanmughapriya S">S Shanmughapriya</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Belibi, F" uniqKey="Belibi F">F Belibi</name></author><author><name sortKey="Zafar, I" uniqKey="Zafar I">I Zafar</name></author><author><name sortKey="Ravichandran, K" uniqKey="Ravichandran K">K Ravichandran</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z Liu</name></author><author><name sortKey="Dai, H" uniqKey="Dai H">H Dai</name></author><author><name sortKey="Jia, G" uniqKey="Jia G">G Jia</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y Li</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author><author><name sortKey="Ren, W" uniqKey="Ren W">W Ren</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Ding, Xue Mei" 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