Clinical evidence indicates that drug resistance is a great obstacle in breast cancer therapy. It renders the disease uncontrollable and causes high mortality. Multiple mechanisms contribute to the development of drug resistance, but the underlying cause is usually a shift in the genetic composition of tumor cells. It is increasingly feasible to engineer the genome with the clustered regularly interspaced short palindromic repeats (CRISPR)/associated (Cas)9 technology recently developed, which might be advantageous in overcoming drug resistance. This article discusses how the CRISPR/Cas9 system might revert resistance gene mutations and identify potential resistance targets in drug-resistant breast cancer. In addition, the challenges that impede the clinical applicability of this technology and highlight the CRISPR/Cas9 systems are presented. The CRISPR/Cas9 system is poised to play an important role in preventing drug resistance in breast cancer therapy and will become an essential tool for personalized medicine.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/advs.201700964

Application of the CRISPR/Cas9 System to Drug Resistance in Breast Cancer.

Estrogens along with their receptors are required for the normal physiological development of women. However,in altered physiological conditions a high level of estrogens acts either as initiator or progressor of breast cancer.Approximately in 75% of estrogen dependent breast cancer cases estrogen receptors (ERs) are held responsible. Recentstudies indicate that estrogens along with iron (Fe) concomitantly involved in the proliferation of ER + breast cancer cells.While a number of antiestrogen/anti-ER drugs including selective estrogen receptor modulators (SERMs), aromatase inhibitors(AIs) and selective estrogen receptor down regulators (SERDs) are used to eradicate breast cancer but their actionon Fe dependent breast cancer complication is not yet explored. Moreover, many of the ER + breast cancer patients receivinganti-estrogen drugs relapsed within a couple of years and become resistant to antiestrogen therapy. Mutation and lossof affinity to the target molecule (ERs), loss or overexpression of ERs, along with activation of growth promoting pathwaysalternative to estrogen-ER pathways are the major reasons of drug resistance. Combinational therapy may be best alternativeto antiestrogen relapsed patients. Some of the widely studied drug combinations are roscovitine (ROSC) and tamoxifen,metformin and tamoxifen, tamoxifen and RAD001. While in all these drug combinations anti-ER compound tamoxifenmay be one of the major content, anti-Fe compounds are yet to be used as drug combination. The present reviewarticle describes all the currently studied drugs/drug combinations in ER + breast cancer cells and future drug possibilitiesincluding anti-Fe compounds.

Mechanistic insight of drug resistance with special focus on iron in estrogen receptor positive breast cancer.

Immunotoxin targeted therapy is a promising way of cancer therapy that is made from a toxin attached to an antibody which target a specific protein presented on cancer cells. In this study, we intr...

Preparation of Diphtheria and Pseudomonas Exotoxin A Immunotoxins and Evaluation of Their Cytotoxicity Effect on SK-BR-3, BT-474, and MDA-MB-231 Breast Cancer Cell Lines.

...................................................................................................................... vi LIST OF TABLES .......................................................................................................... xvii LIST OF FIGURES ....................................................................................................... xviii LIST OF ABBREVIATIONS .......................................................................................... xxi CHAPTER ONE: INTRODUCTION ..................................................................................1 A Brief Overview of Cancer ....................................................................................1 Breast Cancer ...........................................................................................................3 Breast Cancer Metastasis .........................................................................................4 Inflammation in Breast Cancer ................................................................................6 Breast Cancer Subtypes ...........................................................................................7 Breast Cancer Treatment..........................................................................................9 Intracellular Pathways That Promote Breast Cancer Progression .........................10 Oncostatin M and Breast Cancer ...........................................................................11 Interleukin-6, And Interleukin-1 Beta in Breast Cancer ........................................13 Cancer Angiogenesis and Hypoxia Factors ...........................................................14 Circulating Tumor Cells and Their Detection .......................................................15 Mouse Models for Breast Cancer ..........................................................................17 Human Data Analysis ............................................................................................18

/pdf/oncostatin-m-promotes-breast-cancer-metastasis-increased-4vn9tvata7.pdf

Oncostatin M Promotes Breast Cancer Metastasis: Increased Expression of Pro-Angiogenic Factors, Inflammatory Cytokine Expression, and Circulating Tumor Cell Numbers

Catalpol is an iridoid glucoside extracted from the traditional Chinese medicinal plant called Rehmannia glutinosa, and it is reported to possess a variety of pharmacological activities. The goal of this research was to explore the effect of catalpol on the human bladder cancer cells T24. The cells were treated for different durations with various concentrations of catalpol. Then the viability, mobility, and invasiveness of the cells were determined by MTT assay and flow cytometry, respectively. Catalpol was found to significantly suppress the proliferation, migration, and invasiveness of T24 bladder cancer cells in a dose- and time-dependent manner. The results also revealed that catalpol promoted apoptosis and caused the cell-cycle arrest at G2/M phase. Furthermore, the catalpol-mediated apoptosis was found to involve the modulation of PI3K/Akt pathway and inhibit the expression of anti-apoptotic B cell lymphoma-2 (Bcl-2) family proteins. Also, the expressions of Bcl-2 proapoptotic effectors, Bcl-2-associated X protein, and Bcl-2 associated death promoter were up-regulated in the cells treated with catalpol. The enzymes involved in the ultimate process of apoptosis, active caspase-3 and poly ADP ribose polymerase were elevated, and the latter was observed to be cleaved, indicating that catalpol-accelerated cell apoptosis involved a caspase-dependent pathway. These results suggest that catalpol might serve to be a promising therapeutic agent for the treatment of human bladder cancer.

Catalpol Inhibited the Proliferation of T24 Human Bladder Cancer Cells by Inducing Apoptosis Through the Blockade of Akt-Mediated Anti-apoptotic Signaling.

Breast cancer is one of the most common female malignant tumors, with morbidity increasing year by year and age of onset tending to be younger, so its harm cannot be neglected. The HER2/neu gene (also called c-erbB2) coding transmembrane receptor tyrosine protein kinase has an overexpression rate of up to 30% in breast cancer and is closely related to adverse prognosis and low sensitivity to radiotherapy and chemotherapy [1, 2]; therefore targeted therapy against HER-2/neu has become a research hotspot in recent years. Trastuzumab (trade name: Herceptin) is a kind of humanized monoclonal antibody resisting the HER-2/neu gene. In 1998, upon the approval of the Food and Drug Administration (FDA), it was used for the first-line treatment of Her-2 positive advanced breast cancer. Trastuzumab has a good treatment effect on Her-2 positive breast cancer and obviously extends the disease-free survival of patients; however, nearly 50% of Her-2 positive patients are not sensitive to trastuzumab treatment [3]. After 1 year's trastuzumab treatment, most Her-2 positive patients will generate drug resistance to trastuzumab. The drug-resistance mechanism of trastuzumab is relatively complex [4]. The activation of the phosphatidylinositol 3’-kinase/serine-threonine kinase (PI3K/Akt) signal transduction pathway is deemed as one of the important mechanisms of trastuzumab drug resistance [5, 6]. With the important gene p-Akt expression that drug-resistance mechanism might occur to trastuzumab in the PI3K signaling pathway as the entry point and through the inhibition of PI3K/Akt activity of trastuzumab drug-resistance breast cancer cells by its inhibitor LY294002. This research aims to discuss the drug-resistance mechanism of trastuzumab, thus providing a theoretical basis for further improving the treatment effect of breast cancer trastuzumab targeted treatment.

/pdf/research-on-drug-resistance-mechanism-of-trastuzumab-caused-2984547100.pdf

Research on drug resistance mechanism of trastuzumab caused by activation of the PI3K/Akt signaling pathway.

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Research on drug resistance mechanism of trastuzumab caused by activation of the PI3K/Akt signaling pathway.