Natpaphan Yawut
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Natpaphan Yawut has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Sirichat Kaowinn
Department of Cogno-Mechatronics Engineering, Pusan National University, Busan 46241, Republic of Korea
2 shared publications - Young-Hwa Chung
BK21+, Department of Cogno-Mechatronics Engineering, Pusan National University, Busan 609-735, Republic of Korea
2 shared publications - Byeol-Eun Jeon
Department of Integrated Biological Science, Pusan National University, Busan 46241, South Korea
1 shared publication - Chutima Kaewpiboon
Department of Biology, Faculty of Science, Thaksin University, Patthalung 93210, Thailand
1 shared publication - Chutima Kaewpiboon
Department of Biology, Faculty of Science, Thaksin University, Phatthalung, Thailand
1 shared publication - Ho Young Kang
Department of Microbiology, Pusan National University, Busan 46241, Republic of Korea
1 shared publication
Latest Publications
- Open Access
- 30 June 2022
- Published by Korean Society of Cancer Prevention in Journal of Cancer Prevention
- Vol. 27 (2) , 112-121
Formoxanthone C Inhibits Malignant Tumor Phenotypes of Human A549 Multidrug Resistant-cancer Cells through Signal Transducer and Activator of Transcription 1-Histone Deacetylase 4 Signaling
Chutima Kaewpiboon, Nawong Boonnak, Sirichat Kaowinn, Natpaphan Yawut, Young-Hwa Chung. J Cancer Prev 2022;27:112-21. https://doi.org/10.15430/JCP.2022.27.2.112
- 30 June 2022
- Published by Korean Society of Cancer Prevention in Journal of Cancer Prevention
- Vol. 27 (2) , 112-121
Open AccessFormoxanthone C Inhibits Malignant Tumor Phenotypes of Human A549 Multidrug Resistant-cancer Cells through Signal Transducer and Activator of Transcription 1-Histone Deacetylase 4 Signaling
Chutima Kaewpiboon, Nawong Boonnak, Sirichat Kaowinn, Natpaphan Yawut, Young-Hwa Chung. J Cancer Prev 2022;27:112-21. https://doi.org/10.15430/JCP.2022.27.2.112
- Open Access
- 12 January 2022
- Published by MDPI AG in Biomolecules
- Vol. 12 (1) , 122
Elevated Expression of JMJD5 Protein Due to Decreased miR-3656 Levels Contributes to Cancer Stem Cell-Like Phenotypes under Overexpression of Cancer Upregulated Gene 2
Overexpression of cancer upregulated gene (CUG) 2 induces cancer stem cell-like phenotypes, such as enhanced epithelial-mesenchymal transition, sphere formation, and doxorubicin resistance. However, the precise mechanism of CUG2-induced oncogenesis remains unknown. We evaluated the effects of overexpression of CUG2 on microRNA levels using a microRNA microarray. Levels of miR-3656 were decreased when CUG2 was overexpressed; on the basis of this result, we further examined the target proteins of this microRNA. We focused on Jumonji C domain-containing protein 5 (JMJD5), as it has not been previously reported to be targeted by miR-3656. When CUG2 was overexpressed, JMJD5 expression was upregulated compared to that in control cells. A 3′ untranslated region (UTR) assay revealed that an miR-3656 mimic targeted the JMJD5 3′UTR, but the miR-3656 mimic failed to target a mutant JMJD5 3′UTR, indicating that miR-3656 targets the JMJD5 transcript. Administration of the miR-3656 mimic decreased the protein levels of JMD5 according to Western blotting. Additionally, the miR-3656 mimic decreased CUG2-induced cell migration, evasion, and sphere formation and sensitized the cells to doxorubicin. Suppression of JMJD5, with its small interfering RNA, impeded CUG2-induced cancer stem cell-like phenotypes. Thus, overexpression of CUG2 decreases miR-3656 levels, leading to upregulation of JMJD5, eventually contributing to cancer stem cell-like phenotypes.
- 12 January 2022
- Published by MDPI AG in Biomolecules
- Vol. 12 (1) , 122
Open AccessElevated Expression of JMJD5 Protein Due to Decreased miR-3656 Levels Contributes to Cancer Stem Cell-Like Phenotypes under Overexpression of Cancer Upregulated Gene 2
Overexpression of cancer upregulated gene (CUG) 2 induces cancer stem cell-like phenotypes, such as enhanced epithelial-mesenchymal transition, sphere formation, and doxorubicin resistance. However, the precise mechanism of CUG2-induced oncogenesis remains unknown. We evaluated the effects of overexpression of CUG2 on microRNA levels using a microRNA microarray. Levels of miR-3656 were decreased when CUG2 was overexpressed; on the basis of this result, we further examined the target proteins of this microRNA. We focused on Jumonji C domain-containing protein 5 (JMJD5), as it has not been previously reported to be targeted by miR-3656. When CUG2 was overexpressed, JMJD5 expression was upregulated compared to that in control cells. A 3′ untranslated region (UTR) assay revealed that an miR-3656 mimic targeted the JMJD5 3′UTR, but the miR-3656 mimic failed to target a mutant JMJD5 3′UTR, indicating that miR-3656 targets the JMJD5 transcript. Administration of the miR-3656 mimic decreased the protein levels of JMD5 according to Western blotting. Additionally, the miR-3656 mimic decreased CUG2-induced cell migration, evasion, and sphere formation and sensitized the cells to doxorubicin. Suppression of JMJD5, with its small interfering RNA, impeded CUG2-induced cancer stem cell-like phenotypes. Thus, overexpression of CUG2 decreases miR-3656 levels, leading to upregulation of JMJD5, eventually contributing to cancer stem cell-like phenotypes.