Anticancer drugs generally applied to treat breast cancer are taxanes and platinum agents. Taxane drugs involve paclitaxel and docetaxel for BRCA1 gene mutations or hormone-negative cancers. The positive-hormone cancers are significantly less sensitive to taxanes. Hence, platinum agent anticancer drugs like cisplatin and doxorubicin are included as an option to triple-negative breast cancer (lack of estrogen receptors, progesterone receptors, and ERBB2 receptors). Tight junctions (TJs) are structural proteins that control transportation across the cell membrane. These proteins regulate cellular permeability whilst preserving cell polarity, restricting the diffusion of molecules by means of the membrane. Tight junctions also control cellular functions, such as cellular responses to environmental stimuli, intracellular gene expression, cell differentiation, and proliferation. TJs are composed of membrane proteins that can interact with adjacent cells, functioning as a barrier[200,201]. An integral element of TJs that gives structure and function is definitely the protein occludin, encoded by the occludin (OCLN) gene[202,203]. Occludin oxidizes NADH, which can be crucial for TJ morphology, stability, barrier function, and localization of your plasma membrane on endothelial cells. Occludin contains a transmembrane domain with four membrane-spanning regions and other protein domains for example a C-terminus coiled-coil domain to interact with other proteins[200,203]. OCLN’s protein expression can influence the development of numerous cancer kinds, which includes ovarian cancer, lung adenoDNA Methyltransferase list carcinoma[203,205], and breast cancer metastasis. Zhang et al. (2018) reported that OCLN overexpression improved transepithelial resistance, which ALK5 Purity & Documentation indicates stronger TJs, though downregulation of OCLN resulted inside a decreased cell to cell adhesion phenotype (a popular characteristic of tumors). A different study reported that OCLN overexpression stimulates malignant development of lung cancer cells, thereby advertising proliferation and blocking apoptosis. On the other side, eliminating the OCLN gene has been shown to promote tumorigenic things and lessen susceptibility to apoptosis in squamous cell carcinoma. OCLN expression increases on A549 lung cancer cells market their resistance to cisplatin, doxorubicin, and gemcitabine. As an anticancer drug resistance mechanism, there is an increased expression of OCLN inside the TJs of lung cancer cells. The overexpression of OCLN induces drug resistance by inhibiting the flux of doxorubicin, as a result lowering drug concentration within the cell. OCLN might not be connected to cancer drug resistance acquisition directly, nevertheless it limits the chemosensitivity of anticancer drugs to lung cancer cells. Within the A549 lung cancer cell line, OCLN knockdown was not associated straight to their resistance to anticancer drugs, however it suppressed their chemosensitivity on a multicellular spheroid assay. OCLN overexpression on A549 cells decreased doxorubicin permeability resulting from their effect on signaling pathways, lowering the drug’s accumulation and cytotoxicity, leading to anticancer drug resistance. Interestingly, spheroid cancer cells with an elevated OCLN expression developed cisplatin resistance, showing the importance of this gene in MDR.OccludinDRUG DELIVERY SYSTEMS Employing NANOPARTICLES To enhance THE EFFECTIVENESS OF CHEMOTHERAPEUTIC DRUGS IN RESISTANT TUMORSResearchers have adopted various techniques to incorporate carriers to de.