DC Field | Value | Language |
---|---|---|
dc.contributor.author | Bhardwaj, Monika | ko |
dc.contributor.author | Paul, Souren | ko |
dc.contributor.author | Jakhar, Rekha | ko |
dc.contributor.author | Khan, Imran | ko |
dc.contributor.author | Kang, Ji In | ko |
dc.contributor.author | Kim, Ho Min | ko |
dc.contributor.author | Yun, Jong Won | ko |
dc.contributor.author | Lee, Seon-Jin | ko |
dc.contributor.author | Cho, Hee Jun | ko |
dc.contributor.author | Lee, Hee Gu | ko |
dc.contributor.author | Kang, Sun Chul | ko |
dc.date.accessioned | 2018-02-21T06:05:11Z | - |
dc.date.available | 2018-02-21T06:05:11Z | - |
dc.date.created | 2018-02-12 | - |
dc.date.created | 2018-02-12 | - |
dc.date.issued | 2017-12 | - |
dc.identifier.citation | ONCOTARGET, v.8, no.68, pp.112426 - 112441 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | http://hdl.handle.net/10203/240242 | - |
dc.description.abstract | Heat shock transcription factor-1 (HSF-1) guards the cancerous cells proteome against the alterations in protein homeostasis generated by their hostile tumor microenvironment. Contrasting with the classical induction of heat shock proteins, the pro-oncogenic activities of HSF-1 remains to be explored. Therefore, cancer's fragile proteostatic pathway governed by HSF-1 could be a potential therapeutic target and novel biomarker by natural compounds. Vitexin, a natural flavonoid has been documented as a potent anti-tumor agent on various cell lines. However, in the present study, when human colorectal carcinoma HCT-116 cells were exposed to vitexin, the induction of HSF-1 downstream target proteins, such as heat shock proteins were suppressed. We identified HSF-1 as a potential molecular target of vitexin that interact with DNA-binding domain of HSF-1, which inhibited HSF-1 oligomerization and activation (in silico). Consequently, HSF-1 hyperphosphorylation mediated by JNK operation causes transcriptional inactivation of HSF-1, and supported ROS-mediated autophagy induction. Interestingly, in HSF-1 immunoprecipitated and silenced HCT-116 cells, co-expression of apolipoprotein 1 (ApoL1) and JNK was observed which promoted the caspase independent autophagic cell death accompanied by p62 downregulation and increased LC3-I to LC3-II conversion. Finally, in vivo findings confirmed that vitexin suppressed tumor growth through activation of autophagic cascade in HCT-116 xenograft model. Taken together, our study insights a probable novel association between HSF-1 and ApoL-1 was established in this study, which supports HSF-1 as a potential target of vitexin to improve treatment outcome in colorectal cancer. | - |
dc.language | English | - |
dc.publisher | IMPACT JOURNALS LLC | - |
dc.subject | HEAT-SHOCK FACTOR-1 | - |
dc.subject | TRANSCRIPTION FACTOR-1 | - |
dc.subject | SIGNALING PATHWAY | - |
dc.subject | DNA-BINDING | - |
dc.subject | ANTIOXIDANT ACTIVITIES | - |
dc.subject | POTENTIAL ROLE | - |
dc.subject | TUMOR-GROWTH | - |
dc.subject | APOPTOSIS | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | PROTEIN | - |
dc.title | Vitexin confers HSF-1 mediated autophagic cell death by activating JNK and ApoL1 in colorectal carcinoma cells | - |
dc.type | Article | - |
dc.identifier.wosid | 000419569800023 | - |
dc.identifier.scopusid | 2-s2.0-85038824167 | - |
dc.type.rims | ART | - |
dc.citation.volume | 8 | - |
dc.citation.issue | 68 | - |
dc.citation.beginningpage | 112426 | - |
dc.citation.endingpage | 112441 | - |
dc.citation.publicationname | ONCOTARGET | - |
dc.identifier.doi | 10.18632/oncotarget.20113 | - |
dc.contributor.localauthor | Kim, Ho Min | - |
dc.contributor.nonIdAuthor | Bhardwaj, Monika | - |
dc.contributor.nonIdAuthor | Paul, Souren | - |
dc.contributor.nonIdAuthor | Jakhar, Rekha | - |
dc.contributor.nonIdAuthor | Khan, Imran | - |
dc.contributor.nonIdAuthor | Yun, Jong Won | - |
dc.contributor.nonIdAuthor | Lee, Seon-Jin | - |
dc.contributor.nonIdAuthor | Cho, Hee Jun | - |
dc.contributor.nonIdAuthor | Lee, Hee Gu | - |
dc.contributor.nonIdAuthor | Kang, Sun Chul | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | vitexin | - |
dc.subject.keywordAuthor | HSF-1 | - |
dc.subject.keywordAuthor | ApoL1 | - |
dc.subject.keywordAuthor | autophagic cell death | - |
dc.subject.keywordAuthor | colorectal carcinoma | - |
dc.subject.keywordPlus | HEAT-SHOCK FACTOR-1 | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR-1 | - |
dc.subject.keywordPlus | SIGNALING PATHWAY | - |
dc.subject.keywordPlus | DNA-BINDING | - |
dc.subject.keywordPlus | ANTIOXIDANT ACTIVITIES | - |
dc.subject.keywordPlus | POTENTIAL ROLE | - |
dc.subject.keywordPlus | TUMOR-GROWTH | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | PROTEIN | - |
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