Unit V Literature Review

New Data from Southern Medical University Illuminate Findings in Colon Cancer (Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53)

Obesity, Fitness & Wellness Week . (Dec. 9, 2017): p3543.

Copyright: COPYRIGHT 2017 NewsRX LLC

http://www.newsrx.com/newsletters/Obesity,-Fitness-and-Wellness-Week.html

Listen

Full Text: 

2017 DEC 9 (NewsRx) -- By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Research findings on Oncology - Colon Cancer are discussed in a new report. According to news reporting out of Guangzhou, People's Republic of China, by NewsRx editors, research stated, "SETDB1 is a novel histone methyltransferase associated with the functional tri-methylation of histone H3K9. Although aberrant high expression of SETDB1 was experimentally obversed in a variety of solid tumors, its underlying mechanisms in human carcinogenesis are not well known."

Our news journalists obtained a quote from the research from Southern Medical University, "In this study, we investigated the expression of SETDB1 in a large cohort of colorectal cancer (CRC) samples and cell lines for the first time. Our findings showed that SETDB1 was highly expressed in majority CRC tissues and cell lines; moreover, up-regulation of SETDB1 was negatively correlated with the survival rate of CRC patients. Functionally, over-expression of SETDB1 significantly promoted the proliferation and migration of CRC cells and , while knocking down SETDB1 suppressed their growth. Mechanistically, we showed that over-expression of SETDB1 significantly inhibited the apoptosis induced by 5-Fluorouracil in CRC cells, which was closely related to the inhibition of TP53 and BAX expression. Furthermore, we confirmed that SETDB1 could be recruited to the promoter region of TP53, which might contribute its inhibition of apoptosis."

According to the news editors, the research concluded: "For conclusion, our study indicated that SETDB1 is essential for colorectal carcinogenesis, and may be a newly target for treatment and prognostic evaluation in CRC."

For more information on this research see: Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. Journal of Cancer, 2017;8(16):3318-3330. (Springer - www.springer.com; Journal of Cancer - www.springerlink.com/content/0885-8195/)

Our news journalists report that additional information may be obtained by contacting K. Chen, Dept. of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, People's Republic of China. Additional authors for this research include F. Zhang, J. Ding, Y. Liang, Z. Zhan, Y. Zhan, L.H. Chen and Y. Ding.

The direct object identifier (DOI) for that additional information is: https://doi-org.libraryresources.columbiasouthern.edu/10.7150/jca.20482. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.

Keywords for this news article include: Asia, Histones, Oncology, Guangzhou, Colon Cancer, Carcinogenesis, Nucleoproteins, Gastroenterology, Methyltransferases, Colorectal Research, Enzymes and Coenzymes, People's Republic of China, One Carbon Group Transferases.

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2017, NewsRx LLC

The citation for this news report is: NewsRx. New Data from Southern Medical University Illuminate Findings in Colon Cancer (Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53). Obesity, Fitness & Wellness Week. December 9, 2017; p 3543.

Source Citation   (MLA 8th Edition)

"New Data from Southern Medical University Illuminate Findings in Colon Cancer (Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53)." Obesity, Fitness & Wellness Week, 9 Dec. 2017, p. 3543. Health Reference Center Academic, http://link.galegroup.com/apps/doc/A517124430/HRCA?u=oran95108&sid=HRCA&xid=e7b3252d. Accessed 9 Dec. 2017.

Gale Document Number: GALE|A517124430