[4] The production of cytokines allows these cells to escape from the primary tumor and travel through the circulation to distant organs, commencing the process of metastasis.
[5] Due to their significant role in driving disease progression, BCSCs represent a new target by which to treat the tumor at the source of metastasis.
[10] In addition to its ability to promote proliferation and metastasis, the interaction of this protein with osteopontin hastens tumor progression.
[11] ALDH, a family of enzymes that oxidizes intracellular aldehydes and retinol, aids in the differentiation of stem cells.
[14] Such as the interactions between hyaluronic acid (HA) and CD44 stimulate the activation of other pathways that promote tumor malignancy such as Nanog, HER2 and NF-κβ.
As a result, primary breast cancer tumors quickly form metastases in distant sites.
Pathways that play key roles in embryonic development and adult tissue homeostasis have also been implicated in driving the phenotype of BCSCs.
[22] Therapy resistance of BCSCs is mediated by a host of mechanisms, which include ATP-binding cassette transporters, ALDH activity and reactive oxygen species scavenging.