Application of Nanoemulsions in Breast Cancer Treatment

2022 ◽  
pp. 277-306
Author(s):  
M Joyce Nirmala ◽  
Shiny P. J. ◽  
Sindhu Priya Dhas ◽  
Uma Kizhuveetil ◽  
Uppada Sumanth Raj ◽  
...  

A new, efficient, and secure clinical approach is increasingly being sought for the treatment of cancer. Nanoemulsions (NE) are projected to have a profound effect on delivering improved healthcare services with significant implications on forthcoming healthcare policies. In contrast to other drug carriers, the key value of NEs is that they can be engineered to target tumor cells and overcome the major challenge of multi-drug resistance. Multifunctional NEs are being investigated by researchers in various fields of study, primarily in the treatment of different forms of cancer. The congruent presence of NEs with contrast agents or certain dyes increases the accuracy of cancer status identification by enhancing the responsiveness of the agents; thus, they are finding application as nanotheranostics. A summary of different NEs and their documented applications in cancer therapeutics, with emphasis on breast cancer, is presented in this chapter.

2021 ◽  
Vol 27 ◽  
Author(s):  
Ali Sartaj ◽  
Sanjula Baboota ◽  
Javed Ali

Purpose: The available conventional treatment for breast cancer, like surgery, hormonal, radiation, and chemotherapy, given alone or in combination, is commonly used. Due to broad and diverse side effects, toxicity, and multi-drug resistance, chemotherapy has limited use and less effective treatment. In this review, anti-cancer drugs used in combination with phytoconstituents approaches have been summarised. It has been anticipated that this could be a promising and effective strategy for breast cancer treatment. Methods: This review is conducted based on relevant literature using the keywords presented in the title, abstract, and keywords. The available literature search in PubMed, ScienceDirect, MedlinePlus, and Google scholar up to May 2021. A total of 47 articles were selected out of 168 articles based on inclusion and exclusion criteria. Results: The significant drawbacks of available conventional treatment, especially chemotherapy, are low bioavailability for absorption at the specific site of tumor cells, development of multi-drug resistance, and high dose-related to various side effects. The phytoconstituents have anticancerous properties and chemotherapeutic agents that find a promising and potential therapeutics modality. Many in vitro and in vivo studies showed that phytoconstituents could enhance the effectiveness of chemotherapy drugs for breast cancer treatment. Conclusion: The combination approaches of phytoconstituents with chemotherapeutic drugs give less toxicity to normal cells, reduce side effects, and overcome the multi-drug resistance, making the combination approaches an effective strategy.


2021 ◽  
Author(s):  
xingang wang ◽  
YAN ZHENG ◽  
YU WANG

Abstract Background and AimsPseudopodium-enriched atypical kinase 1 (PEAK1) has reported to be upregulated in human malignancies and related with poor prognosis. Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis and chemoresistance. However, the role of PEAK1 in breast cancer is not clear. Here, we investigated the PEAK1 expression in breast cancer and analyzed its relation with clinicopathological status and chemotherapy resistance to the neoadjuvant chemotherapy (NAC). We also investigated the role of PEAK1 on breast cancer cells in vitro and in vivo. MethodsImmunohistochemistry (IHC) was performed in 112 surgical resected breast cancer tissues. The associations between clinicopathological status, multi-drug resistance and PEAK1 expression were determined. Effect of PEAK1 overexpression or down-expression on proliferation, colony formation, invasion, migration, metastasis and Doxorubicin sensitivity in the MCF-7 cells in vitro and in vivo was detected. ResultsPEAK1 was overexpressed in breast cancer tissues and NAC -resistant breast cancer tissues. High PEAK1 expression was related with tumor size, high tumor grade, T stage, LN metastasis, recurrence, Ki-67 expression, Her-2 expression and multi-drug resistance. Targeting PEAK1 inhibited cell growth, invasion, metastasis and reversed chemoresistance to Doxorubicin in breast cancer cells in vitro and in vivo. ConclusionHigh PEAK1 expression was associated with invasion, metastasis and chemoresistance of breast cancers. Furthermore, targeting PEAK1 could inhibit cell growth and metastasis, and reverse chemoresistance in breast cancer cells, which provides an effective treatment strategies for breast cancer.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e15581-e15581
Author(s):  
Yuhao Luo ◽  
Rui Zhou ◽  
Na Huang ◽  
Li Sun ◽  
Wangjun Liao

e15581 Background: Gastric cancer (GC) is a leading cause of cancer mortality worldwide, oxaliplatin and epirubicin based chemotherapy are one of the most important treatment options for GC patients. However, drug resistance, especially multi-drug resistance remains a major obstacle for successful chemotherapy. Recently, long non-coding RNAs (lncRNAs) have been widely identified to play emerging roles in diverse physiological and pathophysiological processes including drug resistance. Our previous bioinformatics analysis showed long non-coding RNA EIF3J-AS1 was a potential multi-drug resistance gene, but the underlying mechanism is still unknown. Methods: We generated oxaliplatin resistance cells (MGC803/OXA) and epirubicin resistance cells(MGC803/EPI) based on parental gastric cancer cells MGC803. Relative expression levels of EIF3J-AS1 were measured by qRT-PCR. Transmission electron microscopy was used to measure autophagosomes. Rapamycin was applied to inducing autophagy while chloroquine and 3-methyladenine were used to block autophagy. Protein level of autophagy related genes were examined by Western Blot. Coexpression genes of EIF3J-AS1 from TCGA RNA-seq datas were analyzed by cBiportal. RNA immunoprecipitation was used to analyze endogenous microRNAs and mRNAs. Results: EIF3J-AS1 was significantly upregulated in MGC803/OXA and MGC803/EPI cells compared with parental cells MGC803. EIF3J-AS1 inhibition increased chemosensitivity to both oxaliplatin and epirubicin. Moreover, EIF3J-AS1 silence lead to the decrease of autophagy. Autophagy related gene ATG14 was identified as a downstream target gene. EIF3J-AS1 promoted ATG14 expression by directly interacting with and increasing stability of ATG14 mRNA, On the other hand, EIF3J-AS1 competitively sponged miR-188-3p and promoted ATG14 expression in a ceRNA-dependent way. Conclusions: LncRNA EIF3J-AS1 is a crucial regulator of multi-drug resistance by inducing autophagy in gastric cancer. Targeting EIF3J-AS1/ATG14 axis might be a new paradigm for cancer therapeutics.


PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0174487 ◽  
Author(s):  
Ching-Ju Shen ◽  
Yu-Ling Kuo ◽  
Chien-Chung Chen ◽  
Ming-Jenn Chen ◽  
Ya-Min Cheng

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Dar-Ren Chen ◽  
Dah-Yuu Lu ◽  
Hui-Yi Lin ◽  
Wei-Lan Yeh

Triple negative breast cancer (TNBC) is an aggressive histological subtype with limited treatment options and a worse clinical outcome compared with other breast cancer subtypes. Doxorubicin is considered to be one of the most effective agents in the treatment of TNBC. Unfortunately, resistance to this agent is common. In some drug-resistant cells, drug efflux is mediated by adenosine triphosphate-dependent membrane transporter termed adenosine triphosphate-binding cassette (ABC) transporter, which can drive the substrates across membranes against concentration gradient. In the tumor microenvironment, upon interaction with mesenchymal stem cells (MSCs), tumor cells exhibit altered biological functions of certain gene clusters, hence increasing stemness of tumor cells, migration ability, angiogenesis, and drug resistance. In our present study, we investigated the mechanism of TNBC drug resistance induced by adipose-derived MSCs. Upon exposure of TNBC to MSC-secreted conditioned medium (CM), noticeable drug resistance against doxorubicin with markedly increased BCRP protein expression was observed. Intracellular doxorubicin accumulation of TNBC was also decreased by MSC-secreted CM. Furthermore, we found that doxorubicin resistance of TNBC was mediated by IL-8 presented in the MSC-secreted CM. These findings may enrich the list of potential targets for overcoming drug resistance induced by MSCs in TNBC patients.


2012 ◽  
Vol 23 ◽  
pp. 56-58 ◽  
Author(s):  
Jing Zhao ◽  
Li Zhu ◽  
Xiaoxi Li ◽  
Bing Bo ◽  
Yongqian Shu ◽  
...  

2017 ◽  
Vol 14 (4) ◽  
pp. 5039-5045 ◽  
Author(s):  
Sergei Boichuk ◽  
Aigul Galembikova ◽  
Alexandr Sitenkov ◽  
Ramil Khusnutdinov ◽  
Pavel Dunaev ◽  
...  

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