Objective (s): In this mini-review, we aimed to discuss the Wnt/β-
catenin signaling pathway modulation in
triple-negative breast cancer, particularly the contribution of lncRNAs and
miRNAs in its regulation and their possible entwining role in
breast cancer pathogenesis, proliferation, migration, or
malignancy. Background: Malignant
tumor formation is very high for
breast cancer in women and is a leading cause of death all over the globe. Among
breast cancer subtypes,
triple-negative breast cancer is rife in premenopausal women, most invasive, and prone to
metastasis. Complex pathways are involved in this
cancer's pathogenesis, advancement, and
malignancy, including the Wnt/β-
catenin signaling pathway. This pathway is conserved among vertebrates and is necessary for sustaining cell homeostasis. It is regulated by several elements such as
transcription factors, enhancers, non-coding RNAs (lncRNAs and
miRNAs), etc. Methods: We evaluated lncRNAs and
miRNAs differentially expressed in
triple-negative breast cancer (TNBC) from the
cDNA microarray data set literature survey. Using in silico analyses combined with a review of the current literature, we anticipated identifying lncRNAs and
miRNAs that might modulate the Wnt/β-
catenin signaling pathway. Result: The
miRNAs and lncRNAs specific to
triple-negative breast cancer have been identified based on literature and database searches.
Tumorigenesis,
metastasis, and EMT were all given special attention. Apart from cross-talk being essential for TNBC
tumorigenesis and treatment outcomes, our results indicated eight upregulated and seven downregulated
miRNAs and 19 upregulated and three downregulated lncRNAs that can be used as predictive or diagnostic markers. This consolidated information could be useful in the clinic and provide a combined literature resource for TNBC researchers working on the Wnt/β-
catenin miRNA/
lncRNA axis. Conclusion: In conclusion, because the Wnt pathway and
miRNAs/lncRNAs can modulate TNBC, their intertwinement results in a cascade of complex reactions that affect TNBC and related processes. Their function in TNBC pathogenesis has been highlighted in molecular processes underlying the
disease progression.