**1. Introduction**

The breast tissue is made up of lobes, adipose tissue, ligaments, cavities (sinuses), glands, and milk ducts. Breast cancer (BC), which develops as a result of excessive cell growth in the breast tissue, is one of the leading causes of mortality after heart and vascular disorders. Although male BC is uncommon, female BC is the most frequent cancer. BC, like all cancers, causes a multitude of DNA abnormalities in healthy cells. As a result, cells begin to multiply uncontrollably. Cancerous cells reproduce and replicate more than healthy cells, and they live much longer. A tumor is defined as an aggregation of cells that results in the creation of a mass [1]. This syndrome frequently occurs in BC as a result of the fast growth of transformed cells in the milk ducts or mammary glands in the breast tissues. Cancer cells that grow in these locations generate a mass known as tumors. BC tumors can be in non-cancerous benign or in cancerous malignant forms. Both forms have varying impacts on the body. Cell growth, which leads to a malignant tumor, is generally gradual in the beginning and does not cause symptoms [2]. Despite advancements in early diagnosis and treatment strategies, metastatic BC continues to be an incurable disease [1].

The spread of malignant BC cells to different human tissues and organs is referred to as BC metastasis. Angiogenesis, invasion, migration, extravasation, and proliferation are a few of the multistep, intricate, and interconnected chains of events that contribute to the development of cancer. By inducing the growth of new blood arteries, tumor cells first break their interactions with surrounding cells and detach from the underlying tumor tissue which is called Epithelial to Mesenchymal Transition (EMT). A primary tumor is one that has formed at the initial location of the tumor. A variety of specific transcription factors, "Epithelial-to-Mesenchymal Transition (EMT) inducers," are at least partially responsible for the complex genetic changes required to achieve EMT-associated phenotypic changes. Snail, Slug, SIP-1, δEF1, E12/E47, and Twist are included in transcription factors that induce EMT. These factors act as transcriptional repressors of E-cadherin in various cell types [1]. In addition, it has been reported to promote EMT by affecting many genes such as matrix metalloproteinase 9 or SPARC in metastasis and cancer invasion. In several cancer models, activation of the transforming growth factor—(TGF) signaling pathway and subsequent upregulation of the EMT inducers Snail, Slug, Twist, and ZEB have been reported to result in EMT [2]. In addition, FOXC2 is a transcriptional factor that promotes EMT and metastasis in vivo. It has been reported that this factor is associated with basal-like cancers [3].

Ten percent of cancer-related deaths are caused by original tumors, but 90% of cancer deaths are caused by metastases, which are secondary cancers that have grown outside the primary tumors. After exiting the main tumor tissue, BC cells move into the extracellular matrix where they advance and either occupy nearby tissues or enter the circulatory system to migrate to distant tissues. Lymph and blood arteries carry them from the main tumor's development site to the metastatic areas. As a result, they survive and reproduce themselves [1, 2]. Because metastasis is a multistep and complex process that includes different steps, due to the heterogeneity of BC, the mechanism of metastasis may diverge from the genetic background of the BC cells. BC has a lot of morphological and molecular heterogeneity not just across tumors, but even within a single tumor. Gene expression profiling allows the identification and classification of major subgroups with varying clinical characteristics and therapeutic responses. The difference between subtypes is caused by three tumor markers: estrogen (ER), progesterone hormone receptors (PR), and human epidermal growth factor receptor 2 (HER2). High levels of hormone receptor expression are observed in luminal A tumors. In addition, the subtype has HER2-negative, ER and/or PR positive, and has low levels of proliferation-related genes. This subtype not only has a modest growth rate, but also a favorable prognosis [1]. BC can show differences in the expression of the hormonal receptors as the result of different genetic alterations and rearrangements within the cell. These differences result in tumor subtypes of BC that show different strategies to survive and invade. Different genomic backgrounds in BC result in genetic variation that shows different mechanisms in cancer progression, especially in metastasis. In this review, metastatic features of BC subtypes are discussed.
