MYC dysfunction modulates stemness and tumorigenesis in breast cancer

As a transcription factor and proto-oncogene, MYC is known to be deregulated in a variety of tumors, including breast cancer. However, no consistent conclusion on the role and mechanism of MYC deregulation during breast cancer carcinogenesis has been formed. Here, we used the UALCAN, bc-GenExMiner, TCGA, cBioportal, STRING and Kaplan-Meier Plotter databases to explore the mRNA expression, prognosis, transcriptional profile changes, signal pathway rewiring and interaction with the cancer stem cells of MYC in breast cancer. We found that the expression of MYC varies in different subtypes of breast cancer, with relatively high frequency in TNBC. As a transcription factor, MYC not only participates in the rewiring of cancer signaling pathways, such as estrogen, WNT, NOTCH and other pathways, but also interacts with cancer stem cells. MYC is significantly positively correlated with breast cancer stem cell markers such as CD44, CD24, and ALDHI. Collectively, our results highlight that MYC plays an important regulatory role in the occurrence of breast cancer, and its amplification can be used as a predictor of diagnosis and prognosis. The interaction between MYC and cancer stem cells may play a crucial role in regulating the initiation and metastasis of breast cancer.

Automated summary

Our study using multiple databases found that MYC expression varies in different subtypes of breast cancer, particularly in TNBC. As a transcription factor, MYC not only participates in rewiring cancer signaling pathways like estrogen, WNT, NOTCH, but also interacts with cancer stem cells. This suggests that MYC plays an important role in breast cancer development and its amplification can serve as a predictor of diagnosis and prognosis.