Abstract
Overexpression of oncogenes and cross-talks of the oncoproteins-regulated signaling cascades with other intracellular pathways in breast cancer could lead to massive abnormal signaling with the consequence of tumorigenesis. The ability to identify the genes having vital roles in cancer development would give a promising therapeutics strategy in combating the disease. Genetic manipulations through siRNAs targeting the complementary sequence of the oncogenic mRNA in breast cancer is one of the promising approaches that can be harnessed to develop more efficient treatments for breast cancer. In this review, we highlighted the effects of major signaling pathways stimulated by oncogene products on breast tumorigenesis and discussed the potential therapeutic strategies for targeted delivery of siRNAs with nanoparticles in suppressing the stimulated signaling pathways.
Highlights
Breast cancer is one of most common life-threatening cancers and the second leading cause of female deaths worldwide
Cross-talks between HER2 and other cell membrane receptors such as estrogen receptor (ER), IGFR, and Epidermal Growth Factor Receptor (EGFR) may initiate downstream signaling through Mitogen-activated protein kinase (MAPK) and PI-3 kinase pathways in breast cancer cells [82], suggesting the importance to determine the genes crucial in the cross-talks for therapeutic purpose
HER2 small interfering RNAs (siRNAs)-based therapeutics delivered using functionalized mesoporous silica nanoparticles coated with a cationic polymer and PEG conjugated to trastuzumab for HER2 targeting was shown to have an excellent safety profile
Summary
Breast cancer is one of most common life-threatening cancers and the second leading cause of female deaths worldwide. Conversion of proto-oncogenes into oncogenes via mutations is one of the prominent causes of the disease, promoting overexpression of growth factor receptors and subsequent cross-talks among their downstream signaling cascades, and can lead to proliferation and survival of cancer cells [11]. Banerjee et al (2011) has shown that Tunicamycin is able to inhibit angiogenesis in vitro and in vivo They have observed reduced expression of vascular endothelial growth factor receptors (VGFRs) and N-glycan in the tumor micro-vessels [21]. Another field of research is immunotherapy, which comprises, for instance, targeting the pathway of programmed death 1/ programmed death ligand. It is crucial to identify key players of the disease’s development and to develop effective therapeutic strategies in targeting breast cancer with or without minimal side effects
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