Cancer cell molecular mimicry of stem cells (SC) follows with enhanced proliferative and renewal capacities. In support, numerous mediators of SC self-renewal have been evinced to exhibit oncogenic potential. More and more researches showed that the embryonic stem cell self-renewal genes express in various cancer cells. In this study, we sought to test the tumorigenic functions of NANOG, particularly, in esophageal cancer (EC). Using quantitative RT-PCR and western blotting, we confirmed that EC cells highly express NANOG mRNA and protein. We then constructed a shRNA-mediated plasmid to knockdown of NANOG mRNA. We observed that NANOG deficiency in Eca109 cells decreased clone formation, cell proliferation, and showed G1 arrest. To further investigate the functions and mechanisms of NANOG in Eca109 cells, we detected the changes of multiple signaling molecules when NANOG deficiency. We foud that NANOG deficiency affected multiple genes, particularly, supressed drug-resistance via down-regulated ABCG2 in Eca109 cells, and caused G1 arrest by down-regulated cyclin D1 (CCND1) expression. The present loss-of-function work, establish the integral role for NANOG in Eca109 cell proliferation, drug resistance, and shed light on its mechanisms of action.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbrc.2017.06.016 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Targeting UBE2T suppresses breast cancer stemness through CBX6-mediated transcriptional repression of SOX2 and NANOG.
Cancer Lett
December 2024
Department of General Surgery, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China; Cuiying Biomedical Research Center, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China; Gansu Province High-Altitude High-Incidence Cancer Biobank, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China. Electronic address:
Breast cancer stem cells (BCSCs) are the main cause of breast cancer recurrence and metastasis. While the ubiquitin-proteasome system contributes to the regulation of BCSC stemness, the underlying mechanisms remain unclear. Here, we identified ubiquitin-conjugating enzyme E2T (UBE2T) as a pivotal ubiquitin enzyme regulating BCSC stemness through systemic screening assays, including single-cell RNA sequencing (scRNA-seq) and stemness-index analysis.
View Article and Find Full Text PDFPressure loading regulates the stemness of liver cancer stem cells via YAP/BMF signaling axis.
J Cell Physiol
October 2024
Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, China.
Cancer stem cells (CSCs) are considered the major cause of the occurrence, progression, chemoresistance/radioresistance, recurrence, and metastasis of cancer. Increased interstitial fluid pressure (IFP) is a key feature of solid tumors. Our previous study showed that the distribution of liver cancer stem cells (LCSCs) correlated with the mechanical heterogeneity within liver cancer tissues.
View Article and Find Full Text PDFOverlapping peri-implantation phenotypes of ZNHIT1 and ZNHIT2 despite distinct functions during early mouse development†.
Biol Reprod
November 2024
Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA, USA.
Article Synopsis
- ZNHIT1 and ZNHIT2 are essential proteins for early mammalian development, and their knockout leads to embryonic lethality during the peri-implantation stage.
- Znhit1 and Znhit2 mutant embryos show overlapping defects, such as reduced SOX2-positive inner cell mass cells and altered expression of critical genes but are impacted by different mechanisms.
- Specifically, ZNHIT1 deficiency disrupts the incorporation of H2A.Z, affecting gene expression for proper trophoblast cell invasion, while ZNHIT2 deficiency results in splicing dysfunction due to lack of EFTUD2.
ETV4 and ETV5 Orchestrate FGF-Mediated Lineage Specification and Epiblast Maturation during Early Mouse Development.
bioRxiv
July 2024
Developmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Article Synopsis
- Cell fate decisions in early mammalian embryos are vital for development, with FGF signaling being crucial but not fully understood in terms of its downstream effects.
- Our study identifies specific transcription factors that are key mediators of FGF signaling, impacting cell lineage specification and maturation in mouse embryos.
- Loss of these factors leads to defects in important developmental processes, suggesting their critical roles in embryonic patterning and overall body plan establishment.
TATA-binding associated factors have distinct roles during early mammalian development.
Dev Biol
July 2024
Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA, USA. Electronic address:
Early embryonic development is a finely orchestrated process that requires precise regulation of gene expression coordinated with morphogenetic events. TATA-box binding protein-associated factors (TAFs), integral components of transcription initiation coactivators like TFIID and SAGA, play a crucial role in this intricate process. Here we show that disruptions in TAF5, TAF12 and TAF13 individually lead to embryonic lethality in the mouse, resulting in overlapping yet distinct phenotypes.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!