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- 저자 : Yawut, Natpaphan (검색결과 3 건)
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Natpaphan Yawut,Sirichat Kaowinn,Il-Rae Cho,Phatcharaporn Budluang,Seonghye Kim,Suhkmann Kim,So Eun Youn,Sang Seok Koh,Young-Hwa Chung 생화학분자생물학회 2022 BMB Reports Vol.55 No.2
Increased mRNA levels of cancer upregulated gene (CUG)2 havebeen detected in many different tumor tissues using Affymetrixmicroarray. Oncogenic capability of the CUG2 gene has beenfurther reported. However, the mechanism by which CUG2overexpression promotes cancer stem cell (CSC)-like phenotypesremains unknown. With recent studies showing that pyruvatekinase muscle 2 (PKM2) is overexpressed in clinical tissues fromgastric, lung, and cervical cancer patients, we hypothesized thatPKM2 might play an important role in CSC-like phenotypes causedby CUG2 overexpression. The present study revealed that PKM2protein levels and translocation of PKM2 into the nucleus wereenhanced in CUG2-overexpressing lung carcinoma A549 andimmortalized bronchial BEAS-2B cells than in control cells. Expressionlevels of c-Myc, CyclinD1, and PKM2 were increasedin CUG2-overexpressing cells than in control cells. Furthermore,EGFR and ERK inhibitors as well as suppression of Yap1 andNEK2 expression reduced PKM2 protein levels. Interestingly,knockdown of β-catenin expression failed to reduce PKM2 proteinlevels. Furthermore, reduction of PKM2 expression with itssiRNA hindered CSC-like phenotypes such as faster wound healing,aggressive transwell migration, and increased size/numberof sphere formation. The introduction of mutant S37A PKM2-greenfluorescence protein (GFP) into cells without ability to move tothe nucleus did not confer CSC-like phenotypes, whereas forcedexpression of wild-type PKM2 promoted such phenotypes. Overall,CUG2-induced increase in the expression of nuclear PKM2contributes to CSC-like phenotypes by upregulating c-Myc andCyclinD1 as a co-activator.
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Kaowinn, Sirichat,Yawut, Natpaphan,Koh, Sang Seok,Chung, Young-Hwa Elsevier 2019 Biochemical and biophysical research communication Vol.511 No.1
<P><B>Abstract</B></P> <P>Although our previous studies have showed that a novel oncogene, cancer upregulated gene (CUG)2 induced epithelial-mesenchymal transition (EMT), the detailed molecular mechanism remains unknown. Because several lines of evidence documented that Yes-Associated Protein (YAP)1 is closely associated with cancer stem cell (CSC)-like phenotypes including EMT, stemness, and drug resistance, we wondered if YAP1 is involved in CUG2-induced EMT. We herein found that the overexpression of CUG2 increased YAP1 expression at the transcriptional as well as protein levels. Chromatin immunoprecipitation assay revealed that the elevated YAP1 transcripts are attributed to c-Jun and AP2 bindings to the YAP1 promoter. Akt and MAPK kinases including ERK, JNK, and p38 MAPK enhanced the level of YAP1 protein. In spite of a close relationship between β-catenin and YAP1, not β-catenin but NEK2 played the role in increasing YAP1 expression. Silencing YAP1 inhibited CUG2-induced cell migration and invasion. N-cadherin and vimentin expressions were decreased during YAP1 knockdown. The suppression of YAP1 diminished TGF-β transcriptional activity and expression as well as phosphorylation level of Smad2 and Twist protein. Conversely, LY2109761 or Smad2 siRNA treatment reduced YAP1 protein levels, indicating a close interplay between YAP1 and TGF-β signaling. Taken together, we suggest that CUG2 induces up-regulation of YAP1 expression, leading to enhancing CUG2-induced EMT via a close crosstalk between YAP1 and TGF-β signaling.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CUG2 enhances expression of YAP1 protein. </LI> <LI> Akt and MAPK kinases are involved in the increase of YAP1 protein expression under overexpression of CUG2. </LI> <LI> Not β-catenin but NEK2 is involved in increase of YAP1 protein expression under overexpression of CUG2. </LI> <LI> YAP1 is involved in CUG2-induced EMT. </LI> </UL> </P>
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Kaewpiboon Chutima,Boonnak Nawong,Kaowinn Sirichat,Yawut Natpaphan,Chung Young-Hwa 대한암예방학회 2022 Journal of cancer prevention Vol.27 No.2
Considering that presence of cancer stem cell (CSC) subpopulation in tumor tissues confers anticancer drug resistance, we investigated whether human A549 lung cancer cells resistant to etoposide possess CSC-like phenotypes. Furthermore, it is known that these malignant tumor features are the leading cause of treatment failure in cancer. We have thus attempted to explore new therapeutic agents from natural products targeting these malignancies. We found that formoxanthone C (XanX), a 1,3,5,6-tetraoxygenated xanthone from Cratoxylum formosum ssp. pruniflorum, at a non-cytotoxic concentration reduced the expression of the signal transducer and activator of transcription 1 (STAT1) and histone deacetylase 4 (HDAC4) proteins, leading to inhibition of CSC-like phenotypes such as cell migration, invasion, and sphere-forming ability. Moreover, we found that treatment with STAT1 or HDAC4 small interfering RNAs significantly hindered these CSC-like phenotypes, indicating that STAT1 and HDAC4 play a role in the malignant tumor features. Taken together, our findings suggest that XanX may be a potential new therapeutic agent targeting malignant lung tumors.
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