*Molecular Mechanisms of Breast Cancer Metastasis DOI: http://dx.doi.org/10.5772/intechopen.108424*

pathways and transcription factors that contribute to stemness can show an insight into this subtype. Notch signaling is a developmental pathway triggered by Notch ligands binding to Notch receptors. Its expression in BC CSCs promotes self-renewal and metastasis. TNBC is significantly deregulated compared to the other BC subtypes. Also, it is found that hypoxia which is a hallmark of TNBC can induce Jagged1, a Notch ligand, expression in TNBC CSCs and lead to metastasis and self-renewal. PKD3 is part of the protein kinase D (PKD) family and is shown to have a role in increasing TNBC metastasis, proliferation, and stemness. Another pathway that is linked to the increased risk of metastasis in TNBC is the Interleukin/Janus kinase-2/ signal transducer and activators of transcription-3 (IL-6/JAK2/STAT3) pathway and it is preferentially activated in TNBC CSCs comparing to the other BC subtypes. SRY-box transcription factor 2 (*SOX2*) is a stem cell pluripotency regulator which is effective in embryonic development and it is over-expressed in TNBC. This expression level of *SOX2* is associated with increased proliferation and metastasis. Further, Lipase H (*LIPH*) is found to regulate *SOX2* so it is another gene to promote metastasis in TNBC CSCs. *NANOG* is known to be a self-renewal and pluripotency regulator and it is also found to be a key driver of metastasis too. Ubiquitin carboxyl-terminal hydrolase 1 (*USP1*) and Protocadherin-7 (*PCDH7*) were also found to be promoting metastasis in TNBC CSCs. And finally, under the list of epigenetic regulation, histone methyltransferase *EZH2* was found to maintain metastasis in TNBC CSCs [85].
