MSX2

Official Full Name

msh homeobox 2

Organism

Homo sapiens

GeneID

4488

Background

This gene encodes a member of the muscle segment homeobox gene family. The encoded protein is a transcriptional repressor whose normal activity may establish a balance between survival and apoptosis of neural crest-derived cells required for proper craniofacial morphogenesis. The encoded protein may also have a role in promoting cell growth under certain conditions and may be an important target for the RAS signaling pathways. Mutations in this gene are associated with parietal foramina 1 and craniosynostosis type 2. [provided by RefSeq, Jul 2008]

Synonyms

FPP; MSH; PFM; CRS2; HOX8; PFM1;

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Detailed Information

The MSX2 gene is a member of the sarcomeric homeobox gene family, which encodes a transcriptional repressor that regulates cell survival and apoptosis. There are two subtypes of MSX1 and MSX2 in human cells, and three subtypes of MSX1, MSX2 and MSX3 in rodents. MSX2 is expressed in the process of embryogenesis and organogenesis, and controls cell proliferation and differentiation in vivo. It is expressed in various tissues and organs such as cranial nerve spasm, breast, neural tube, tooth germ, eye, ear, nose, pituitary, heart, bone, and brain. However, abnormal expression or mutation of MSX2 may have adverse effects on the body. MSX2 mutations are associated with human neural tube defects. MSX2 mutations can cause BOSTON-type craniopharyngioma and craniosynostosis. In addition, abnormal expression of the MSX2 gene was also found in gastric cancer, ovarian cancer, and lung cancer cells.

Figure 1. MicroRNAs suppress the osteogenic differentiation of mesenchymal stem cells through targeting transcription factors RUNX2, Smuf1, Osterix or BMP protein. (Peng, S., et al. 2016)

MSX2 and EMT

MSX2 and EMT play a crucial role in epithelial-mesenchymal transitions in the development of tumors. The study found that in the pancreatic cancer cells transfected with MSX2, the intercellular connections were found to be loose, and E-cadherin and β-catenin, which were originally localized in the cell membrane, were dispersed in the cytoplasm. The expression of E-cadherin was down-regulated by western-blot, the expression of β-catenin was up-regulated in the nucleus and stroma, and the expression of β-catenin was down-regulated, and EMT was observed in the cells. In this study, Twist1 expression was also up-regulated in BXPC3 cells with high expression of MSX2, whereas Twist1 was decreased in PANC-1 cells with low expression of MSX2. Twist1 was consistent with the expression of MSX2 in pancreatic cancer by immunohistochemical analysis. This suggests that Twist1 may be a target gene for MSX2, and it is speculated that MSX2 may promote EMT through Twist1 in pancreatic cancer, thereby increasing its malignant phenotype.

The study found that ovarian cancer cells IOSE80, PEO4 and OVCA433 transfected with MSX2 showed varying degrees of fibroblast-like morphological changes and showed EMT. The study found that MSX2 was introduced into mouse mammary epithelial cells NMuMG, epithelial marker molecules. The expression of E-cadherin was down-regulated and the expression of the interstitial marker vimentin and N-cadherin was up-regulated. It was also detected that the Cripto-1 expression of the epidermal growth factor CFC family was up-regulated with the increase of MSX2, and knockout Cripto-1 could make it high. Expression of E-cadherin in MSX2 mammary epithelial cells is upregulated, and DiBari speculates that MSX2 promotes EMT in mammary epithelial cells via Cripto-1. These studies suggest that MSX2 plays an important role in tumor cell EMT and that its mechanisms may be different in different tissues.

MSX2 and Tumor

Malignant proliferation of normal cells is the beginning of tumor formation, and MSX2 plays a role in this process. The study found that the HPDE (human pancreatic ductal epithelial) cells transfected with MSX2 were more than 2.5 times more proliferative than the untransfected cells. The study also found that the proliferation of BXPC3 cells with high expression of MSX2 was much higher than that of B-3EV with low expression of MSX2. This indicates that MSX2 has a role in promoting pancreatic cell proliferation, whether it is normal pancreatic ductal cells (HPDE) or cancer cells (BXPC3). Cell proliferation was inhibited after knockdown of the MSX2 gene in ovarian cancer cells TOV112D and TOV21G, and ovarian cancer growth restriction was also confirmed in nude mice after knockout of MSX2. In odontogenic tumors, AMBN was inhibited by heparin-binding domain Ameloblastoma proliferate, and this process is accompanied by down-regulation of MSX2, which indirectly indicates the role of MSX2 in promoting the proliferation of ameloblastoma. MSX2 has also been found to promote cell proliferation in mammary epithelial cells, and this effect is affected by ovarian hormones.

References:

Peng, S. , Gao, D. , Gao, C. , Wei, P. , Niu, M. , & Shuai, C. . (2016). Micrornas regulate signaling pathways in osteogenic differentiation of mesenchymal stem cells (review). Molecular Medicine Reports.
Haddaji Mastouri, M. , De Coster, P. , Zaghabani, A. , Jammali, F. , Raouahi, N. , & Ben Salem, A. , et al. (2017). Genetic study of non-syndromic tooth agenesis through the screening of paired box 9, msh homeobox 1, axin 2, and wnt family member 10a genes: a case-series. European Journal of Oral Sciences.
Taghiyar, L. , Hesaraki, M. , Sayahpour, F. A. , Satarian, L. , Hosseini, S. , & Aghdami, N. , et al. (2017). Msh homeobox 1 (msx1)- and msx2-overexpressing bone marrow-derived mesenchymal stem cells resemble blastema cells and enhance regeneration in mice. Journal of Biological Chemistry, 292(25), jbc.M116.774265.

Quick Inquiry

Interested in learning more?

Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.

Request a quote today!

Inquiry