S100A4, AN IMPORTANT TARGET FOR SURE! LOCATED AT 1q21

The importance of a molecule in the body is determined  by its chemical properties, the pathogenesis of the disease in which it is  participating or how critical a function it is performing in the cascade of a pathway. The importance of a gene is determined by its product's shape and function which is sometimes defined by atoms hanging at its periphery, ready for business of attracting other electrons or ions.  It is also determined by genes in a linkage relationship at the chromosome level. This last point is important to be clarified by researchers who have the tools to explore the coexistence of genes on an arm of a specific chromosome.  And a lot of research forgets to look at that aspect of the problem gene. (don't forget "q" most of the time portends for worse prognosis than "p" , that is it may induce a malignant phenotype.  In fact, co-expression of homologue "p" will mitigate the phenotype. And the homologue gene is on a p arm and on a different numbered chromosome)

By now you also know that cell life is directed in one direction at a time frequently.  Cells are under function performance, differentiation, proliferation or neoplastic transformation.  Neoplastic cells are in concert with surrounding cells from which it avoids to be in conflict with to escape detection.  Neoplastic Cells will be soon stressed because of their increased needs and through the c-JUN -FOS will increase a Tumor Growth factor liberated from the cellular membrane with concomittent release of Metalloproteases in the extracellular membrane through flippase-floppase activity.  The Metalloprotease goes out, the Growth factor goes in.
IT WOULD BE GOOD TO KNOW WHICH METALLOPROTEASE IS SPECIFICALLY LINKED TO WHICH PROTEIN IN ORDER TO KNOW WHAT IS GOING ON INSIDE THE CELL JUNK BY DETERMINING WHICH OF THE METALLOPROTEASE   FAMILY MEMBER IS IN THE EXTRACELLULAR SPACE OR BLOOD!   NICE LITTLE PROJECT RIGHT THERE.  "WHICH TYPE OF METALLOPROTEASE FOR WHICH CANCER"  I BET, BRAIN TUMOR WILL RELEASE A DIFFERENT METALLOPROTEASE THAN OVARIAN CANCER.  BECAUSE THE GROWTH HORMONE RELEASED IN THE CELL WILL BE DIFFERENT.

By now you also know that in certain proliferative processes, there is an increased aspect of only 1 or 2 functions.  In Leukemias, for example, it is amplification of a certain Core binding complex which attaches certain molecules with specific functions.  And the cell follows the cascade of functions to go in a certain cell life trend.  Some of these proteins are gene regulators.  In fact, Leukemia would be better controlled if we just determined the proteins on CBF and the regulators that are promoted in the cell.  ANOTHER EASY PROJECT : THE PATTERNS OF GENE REGULATORS IN A SPECIFIC LEUKEMIA (BY WETERN OR SOUTHERN BLOT).

One of those regulators is the S100A4, a potent regulator which not only is at the differentiation, meaning when mutated or amplified it will create phenotypic havoc for sure.  It is handling Calcium, therefore will affect some Microtubules (good or bad for Taxanes?):  Time to find out more! Read these articles!

1. High expression of S100A4 in cytoplasm at the advancing front of stage C colonic tumours indicates a poor prognosis.
2. The S100A4 protein, mostly studied in cancer, is overexpressed in the damaged human and rodent brain and released from stressed astrocytes.
3. we show for the first time the intratumoral knock down of S100A4 via systemic application of S100A4shRNA plasmid DNA, restricts metastasis formation in a xenografted mouse model of colorectal cancer.
4. SRX forms a complex with S100A4 (and has stronger affinity for S-glutathionylated S100A4), regulates its activity, and mediates redox regulation of the interaction of S100A4 with nonmuscle myosin heavy chain II-A.
5. S100A4 and its downstream factors play important roles in pancreatic cancer invasion, and silencing A100A4 can significantly contain the invasiveness of pancreatic cancer.
6. HBXIP up-regulates S100A4 through activating S100A4 promoter involving STAT4 and inducing PTEN/PI3K/AKT signaling to promote growth and migration of breast cancer cells.
7. S100A4 and VEGF mRNA levels were up-regulated in clear cell renal cell carcinoma (CCRCC), tissue compared with control; upregulated tumour S100A4 and VEGF mRNA levels were independent risk factors for the presence of invasion and/or metastasis
8. High S100A4 is associated with ovarian cancer invasiveness.
9. FSP1 localized to podocytes in focal segmental glomerulosclerosis & minimal change disease. The number of FSP1(+) podocytes per glomerular profile was higher in patients with FSGS than in MCD. There was a corresponding difference in FSP1 mRNA levels.
10. Asymmetric mode of Ca-S100A4 interaction with nonmuscle myosin IIA generates nanomolar affinity required for filament remodeling in epithelial carcinoma cells.

NOTE HBXIP S100A4:  AN IMPORTANT TARGET FOR CERTAIN!