Female breast cancer has outstripped lung cancer to be the most diagnosed malignancy worldwide. Recently, abnormality in DNA replication licensing caused by dysregulation of minichromosome maintenance proteins (MCMs) has been shown to involve in the initiation, development, and metastasis of multiple malignancies via destabilizing genomic replication. MCM10, a member of the MCMs family proteins, is crucial for the initiation of DNA replication and high expression of MCM10 is observed in various cancers. However, MCM10 association with breast cancer and precise mechanisms remain largely unexplored. In the present research, we have used a combination of different in-silico, in-vitro, ex-vivo, biochemical, and mass spectrometry techniques, to explore the association of MCM10 with breast cancer malignancy. We found high expression of MCM10 in a variety of cancers compare to their normal tissues. In clinical breast cancer patients, we observed that expression levels of MCM10 protein are strongly associated with the degree of breast cancer aggressiveness. Mechanically, we found that overexpression of MCM10 promotes tumorigenic properties in non-tumorigenic mammary cells. High expression ofMCM10 increased proliferation by shortening the S-phase in the cell cycle and activating the AKT signaling pathway. Moreover, overexpression of MCM10 is found to induce DNA replication catastrophe by the accumulation of ssDNA and subsequently overexpression of ssDNA binding protein RPA. Furthermore, we observed, MCM10 when overexpressed interacts with a substantial number of different proteins compared to the normal conditions. Genomic and proteomic analysis of MCM10 interactions that are possibly be involved in breast cancer progression revealed high expression of these MCM10 interacting partners on mRNA and protein levels in breast cancer patients. In addition, overexpression of MCM10 in non-tumorigenic mammary cells also resulted in promoting tumorigenic characters in in-vivo mimicking conditions. Mesenchymal markers such as up-regulation of VIMENTIN, transcription factor SNAIL and TWIST2, and the down-regulation of E-CADHERIN were observed in MCM10 overexpression cells. Cumulatively, we envision MCM10 being both, a potential clinical therapeutic target for breast cancer treatment and a potential fingerprint in discriminating different degrees of breast cancer malignancy, which ultimately can reduce the overall burden posed by this devastating disease.