SOME GENES OF METASTASIS

1. miR 126
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This gene is the center of Metastatic progression of disease, It is the agent of cellular entrance in vessels to start migration.  Activation of miR126 start the metastatic process by controlling events at the cellular membranes by acting on the CRK.  Should the cell need more time to engage in multiplication before seeding, it uses IRS-1 to block cell division.  By SPRED-1, TOM1, VEGF-A and PIK3-R2, it modulates formation of proper vascular channel through which  cancer cell can penetrate blood vessel or vessels in general without leak.  Remember cavalier tampering with blood vessel leads to leaks recognized as a risk in the use of Avastin.  Same danger recognized in squamous cell lung cancer with the use of certain anti-VEGF.
It also serve as a general amplifier of all Metastatic genes (HOX9).
It even modulates defense cells. (inhibition of GATA3 through POU3F1)
It has been seen in almost all solid tumors and hematologic malignancies.
and is predictive of Metastasis....

miR 126, a huge target during maintenance therapy.  No miR 126, No embryogenesis!

2.  miR 335
---------------------(there are 750 miR recognized from various species) This one is also common in human cancers.

3. TWIST-1
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 The family of TWIST but particularly transcription factor TWIST-1, has been implicated in cell lineage and differentiation. It allows the cell to cope with Hypoxia and to resist Cisplatin attacks.  In Metastasis it seems to participate in the upregulation of Metalloproteases, the enzymes that breaks tissue collagens and fibronectin, opening up the road to Migration.   Of note, Concurrent upregulation of MYC and TWIST-1 have been detected in Neuroblastoma.  The most important function is through its interaction with K-RAS. This is where TWIST-1 shuts down senescence which could lead to Apoptosis.  Knocking down TWIST-1 seems to put back the cell through its maturation track.  This target can be important in Leukemia in theory.
There is a Notch1/STAT3/TWIST-1/KRAS/EP300 axis here which some how is totally anti-apoptosis through blockage of natural aging of cancerous cell.  This has been in worse types of lung cancer.
Through its interaction with EP300, PCAF, it activates the NOTCH-1 and through TCF3, it amplify differentiation and metastasis.

TWIST-1 cause cell detachment by decreasing Claudin4
TWIST-1 shuts cell division by increasing Bmi-1

4. SNA  11, and 12
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5. MACC-1 in Colon cancer
--------------------------  "MACC1 is a key regulator of the hepatocyte growth factor (HGF; MIM 142409)-HGF receptor (HGFR, or MET; MIM 164860) pathway, which is involved in cellular growth, epithelial-mesenchymal transition, angiogenesis, cell motility, invasiveness, and metastasis. Expression of MACC1 in colon cancer (MIM 114500) specimens is an independent prognostic indicator for metastasis formation and metastasis-free survival (Stein et al., 2009 [PubMed 19098908]).[supplied by OMIM, Mar 2009]"

Mesenchymal expression in any cancer is bad sign but in this particular case this point to adaptation to invaded tissue and its tendency to migrate as if in embryonal state to where these receptors are with seeding intentions!

HGFR -MET will promote angigenesis and is the very reason Avastin is advised in Metastatic colon cancer. And support the idea of "Maintenance therapy" or continued Avastin in progression of diseases. 

Presence of MACC-1 and its amplification c-MET are the underlying reason for the success of Nexavar in Hepatocellular cancer where Cabozantinib will certainly have a role!


6. Methaderin in Breast cancer
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Wikipedia says it better:

"'Function

AEG-1 is involved in HIF-1alpha mediated angiogenesis. AEG-1 also interacts with SND1 and involved in RNA-induced silencing complex (RISC) and plays very important role in RISC and miRNA functions.^[4][5]
AEG-1 induces an oncogene called Late SV40 factor (LSF/TFCP2) which is involved in thymidylate synthase (TS) induction and DNA biosynthesis synthesis.^[6] Late SV40 factor (LSF/TFCP2) enhances angiogenesis by transcriptionally up-regulating matrix metalloproteinase-9 (MMP9).^[7]

Clinical significance

AEG-1 acts as an oncogene in melanoma, malignant glioma, breast cancer and hepatocellular carcinoma.^[8] It is highly expressed in these cancers and helps in progression and development of these cancers. It is induced by c-Myc oncogene and plays very important role in anchorage independent growth of cancer cells.
Elevated expression of the metastasis gene metadherin (MTDH), which is overexpressed in more than 40% of breast cancers, is associated with poor clinical outcomes. MTDH has a dual role in promoting metastatic seeding and enhancing chemoresistance. MTDH is therefore a potential therapeutic target for enhancing chemotherapy and reducing metastasis.^[9]
LSF/TFCP2 plays multifaceted role in chemo resistance, EMT, allergic response, inflammation and Alzheimer’s disease.^[10]
AEG-1 controls many hallmarks of oncogenes and cancer. AEG-1/MTDH induces hepato steatosis in mouse liver.^[11] The MTDH knockdown by artificial microRNA interference functions as a potential tumor suppressor in breast cancer.^[12] Astrocyte elevated gene-1/MTDH undergoes palmitoylation in normal and abnormal physiology of the cell [13].The microgrooved biomaterial titanium substrata can alter the expression of AEG-1 in human primary cells [14]."

 Wikipedia says it best:
Discovered at Princeton, present in 30-40% of breast cancers.


7. InterLeukin -11 and PTHR   in seeding into the bones:
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8. Role of Hepatocyte Growth Factor receptors
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9. Role OF DEATH RECEPTOR 3:  apparantly by exocytosis, these molecules are thrown into the extra cellular Matrix to play a role of Decoy fooling cellular defense from the neighboring cell

10. ROLE OF RECEPTORS, CLA,LFA-1,CCR-4, CXR-4,Fas, p15, p16

11. Eph-A4: This receptor has a role in cell development.  It actually receives molecule or ligand for the neighboring cell. and depend on the ligand (Ephrin Vs others) it know where and when to migrate.  It is critical to the development of the central Nervous system.  researcher have look at this receptor for development of Melanoma therapy. some Blockers at this receptors may promote Axonal regeneration

Others UNDER REVIEW AT CRBCM.
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Group 1 :    CCL-5, EREG,  MMP-1, LOX, PTGS, ANGPTL-4,
Group_2:   CSF2RB, MET,D1
Grooup 3:  KISS-1,DARC,GPR, ERBB2,CTNNB1

12. METALLOPROTEASES, AND THEIR RECEPTORS IN METASTASIS.

13. INTEGRINS, ICAM-2, E-CADHERINS, SIALYL LEWIS CARBOHYDRATES, SELECTINS P AND E.