Alternative splicing in breast cancer

Alternative splicing allows a gene to produce multiple proteins and is the main source of human proteome diversity. Aberrant regulation of alternative splicing produces proteins with different structures and can lead to altered protein function, inactivation, or deleterious variants, which can have severe effects on normal cellular function, leading to many diseases, including cancer. Alternative splicing abnormalities are often found in diseases, so alternative splicing is highly correlated with diseases and treatment. According to relevant statistics, breast cancer is an important factor that threatens women's lives and health. A common sign of tumors in humans is abnormal alternative splicing. An increasing amount of evidence shows that abnormal alternative splicing plays an important role in the occurrence and development of breast cancer. At the same time, in the related treatment of breast cancer, alternative splicing can lead to the failure of existing treatment methods and induce drug resistance. Currently, targeted therapy is still the key strategy for breast cancer treatment. In this review, we discuss the five classifications of alternative splicing and aberrant alternative splicing in breast cancer. The role of alternative splicing in the drug resistance of breast cancer is also discussed. Evidence has shown that aberrant alternative splicing can lead to drug resistance to current therapies. Because splicing factors are involved in many aspects of cancer, splicing factors may provide a new strategy for cancer treatment and a powerful tool for progress in the fight against breast cancer. Antisense oligonucleotides form a double-stranded structure by complementary pairing with mRNA, which prevents the binding of mRNA and ribosomes, thus inhibiting protein synthesis. Therefore, after finding effective targets, antisense oligonucleotides can be applied in gene therapy, drug research and development, biological research, and other fields to improve therapeutic effects.