scholarly journals The importance of epithelial-mesenchymal transition and autophagy in cancer drug resistance

2019 ◽  
Author(s):  
Charlotte Hill ◽  
Yihua Wang
Keyword(s):  
Drug Resistance ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Drug ◽  
Mesenchymal Transition ◽  
Cancer Drug Resistance

scholarly journals A Novel Model of Cancer Drug Resistance: Oncosomal Release of Cytotoxic and Antibody-Based Drugs

Biology ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 47 ◽  
Author(s):  
Takanori Eguchi ◽  
Eman Ahmed Taha ◽  
Stuart K. Calderwood ◽  
Kisho Ono
Keyword(s):  
Drug Resistance ◽  
Tumor Cells ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Drug ◽  
Cell Phenotype ◽  
Mesenchymal Transition ◽  
Cancer Drug Resistance ◽  
Anti Cancer ◽  
Secretory Phenotype ◽  
Novel Model

Extracellular vesicles (EVs), such as exosomes or oncosomes, often carry oncogenic molecules derived from tumor cells. In addition, accumulating evidence indicates that tumor cells can eject anti-cancer drugs such as chemotherapeutics and targeted drugs within EVs, a novel mechanism of drug resistance. The EV-releasing drug resistance phenotype is often coupled with cellular dedifferentiation and transformation in cells undergoing epithelial-mesenchymal transition (EMT), and the adoption of a cancer stem cell phenotype. The release of EVs is also involved in immunosuppression. Herein, we address different aspects by which EVs modulate the tumor microenvironment to become resistant to anticancer and antibody-based drugs, as well as the concept of the resistance-associated secretory phenotype (RASP).

Quest of EMT and CSC

2019 ◽  
Author(s):  
Shihori Tanabe
Keyword(s):  
Drug Resistance ◽  
Stem Cell ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Therapeutics ◽  
Cancer Drug ◽  
Phenotypic Change ◽  
Mesenchymal Transition ◽  
Cancer Drug Resistance ◽  
The Relationship

Epithelial-mesenchymal transition (EMT), an important phenotypic change from epithelial to mesenchymal like cells, has the increasing impact for cancer progression in terms of the involvement in cancer stem cell (CSC). The EMT-featured cells and CSCs are important factors for the acquisition of cancer drug resistance. The understanding of EMT program activation is important for targeting CSCs in cancer therapy. The relationship between EMT and CSC in cancer therapeutics is focused in the editorial.

scholarly journals The role of epithelial–mesenchymal transition-regulating transcription factors in anti-cancer drug resistance

2021 ◽  
Author(s):  
Jihye Seo ◽  
Jain Ha ◽  
Eunjeong Kang ◽  
Sayeon Cho
Keyword(s):  
Drug Resistance ◽  
Transcription Factors ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Drug ◽  
Preclinical Studies ◽  
Mesenchymal Transition ◽  
Cancer Drug Resistance ◽  
Anti Cancer ◽  
Future Challenges

AbstractThe complex orchestration of gene expression that mediates the transition of epithelial cells into mesenchymal cells is implicated in cancer development and metastasis. As the primary regulator of the process, epithelial-mesenchymal transition-regulating transcription factors (EMT-TFs) play key roles in metastasis. They are also highlighted in recent preclinical studies on resistance to cancer therapy. This review describes the role of three main EMT-TFs, including Snail, Twist1, and zinc-finger E homeobox-binding 1 (ZEB1), relating to drug resistance and current possible approaches for future challenges targeting EMT-TFs.

scholarly journals Exosomes and breast cancer drug resistance

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Xingli Dong ◽  
Xupeng Bai ◽  
Jie Ni ◽  
Hao Zhang ◽  
Wei Duan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Drug ◽  
Therapeutic Drug ◽  
Mesenchymal Transition ◽  
Cancer Drug Resistance ◽  
Survival Signaling ◽  
Daunting Challenge

AbstractDrug resistance is a daunting challenge in the treatment of breast cancer (BC). Exosomes, as intercellular communicative vectors in the tumor microenvironment, play an important role in BC progression. With the in-depth understanding of tumor heterogeneity, an emerging role of exosomes in drug resistance has attracted extensive attention. The functional proteins or non-coding RNAs contained in exosomes secreted from tumor and stromal cells mediate drug resistance by regulating drug efflux and metabolism, pro-survival signaling, epithelial–mesenchymal transition, stem-like property, and tumor microenvironmental remodeling. In this review, we summarize the underlying associations between exosomes and drug resistance of BC and discuss the unique biogenesis of exosomes, the change of exosome cargo, and the pattern of release by BC cells in response to drug treatment. Moreover, we propose exosome as a candidate biomarker in predicting and monitoring the therapeutic drug response of BC and as a potential target or carrier to reverse the drug resistance of BC.

The Potential for Natural Products to Overcome Cancer Drug Resistance by Modulation of Epithelial-Mesenchymal Transition

2022 ◽  
pp. 1-27
Author(s):  
Asefeh Dahmardeh Ghalehno ◽  
Arad Boustan ◽  
Hakimeh Abdi ◽  
Zahra Aganj ◽  
Fatemeh Mosaffa ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Natural Products ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Drug ◽  
Mesenchymal Transition ◽  
Cancer Drug Resistance

scholarly journals Epitranscriptomics and epiproteomics in cancer drug resistance: therapeutic implications

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Huibin Song ◽  
Dongcheng Liu ◽  
Shaowei Dong ◽  
Leli Zeng ◽  
Zhuoxun Wu ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Posttranslational Modification ◽  
Drug Target ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Drug ◽  
Chemotherapeutic Drugs ◽  
Mesenchymal Transition ◽  
Therapeutic Implications ◽  
Cancer Drug Resistance ◽  
Damage Repair

Abstract Drug resistance is a major hurdle in cancer treatment and a key cause of poor prognosis. Epitranscriptomics and epiproteomics are crucial in cell proliferation, migration, invasion, and epithelial–mesenchymal transition. In recent years, epitranscriptomic and epiproteomic modification has been investigated on their roles in overcoming drug resistance. In this review article, we summarized the recent progress in overcoming cancer drug resistance in three novel aspects: (i) mRNA modification, which includes alternative splicing, A-to-I modification and mRNA methylation; (ii) noncoding RNAs modification, which involves miRNAs, lncRNAs, and circRNAs; and (iii) posttranslational modification on molecules encompasses drug inactivation/efflux, drug target modifications, DNA damage repair, cell death resistance, EMT, and metastasis. In addition, we discussed the therapeutic implications of targeting some classical chemotherapeutic drugs such as cisplatin, 5-fluorouridine, and gefitinib via these modifications. Taken together, this review highlights the importance of epitranscriptomic and epiproteomic modification in cancer drug resistance and provides new insights on potential therapeutic targets to reverse cancer drug resistance.

scholarly journals Chronic TGF-β exposure drives stabilized EMT, tumor stemness, and cancer drug resistance with vulnerability to bitopic mTOR inhibition

2019 ◽  
Vol 12 (570) ◽  
pp. eaau8544 ◽  
Author(s):  
Yoko Katsuno ◽  
Dominique Stephan Meyer ◽  
Ziyang Zhang ◽  
Kevan M. Shokat ◽  
Rosemary J. Akhurst ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Progression ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Carcinoma Cells ◽  
Cancer Drug ◽  
Mtor Inhibition ◽  
Mesenchymal Transition

Tumors comprise cancer stem cells (CSCs) and their heterogeneous progeny within a stromal microenvironment. In response to transforming growth factor–β (TGF-β), epithelial and carcinoma cells undergo a partial or complete epithelial-mesenchymal transition (EMT), which contributes to cancer progression. This process is seen as reversible because cells revert to an epithelial phenotype upon TGF-β removal. However, we found that prolonged TGF-β exposure, mimicking the state of in vivo carcinomas, promotes stable EMT in mammary epithelial and carcinoma cells, in contrast to the reversible EMT induced by a shorter exposure. The stabilized EMT was accompanied by stably enhanced stem cell generation and anticancer drug resistance. Furthermore, prolonged TGF-β exposure enhanced mammalian target of rapamycin (mTOR) signaling. A bitopic mTOR inhibitor repressed CSC generation, anchorage independence, cell survival, and chemoresistance and efficiently inhibited tumorigenesis in mice. These results reveal a role for mTOR in the stabilization of stemness and drug resistance of breast cancer cells and position mTOR inhibition as a treatment strategy to target CSCs.

Fanconi Anemia DNA Repair Pathway as a New Mechanism to Exploit Cancer Drug Resistance

2020 ◽  
Vol 20 (9) ◽  
pp. 779-787
Author(s):  
Kajal Ghosal ◽  
Christian Agatemor ◽  
Richard I. Han ◽  
Amy T. Ku ◽  
Sabu Thomas ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Dna Repair ◽  
Fanconi Anemia ◽  
Cancer Drug ◽  
Drug Resistant ◽  
Cancer Drugs ◽  
Repair Pathway ◽  
Cancer Drug Resistance ◽  
Anti Cancer ◽  
Cancerous Cells

Chemotherapy employs anti-cancer drugs to stop the growth of cancerous cells, but one common obstacle to the success is the development of chemoresistance, which leads to failure of the previously effective anti-cancer drugs. Resistance arises from different mechanistic pathways, and in this critical review, we focus on the Fanconi Anemia (FA) pathway in chemoresistance. This pathway has yet to be intensively researched by mainstream cancer researchers. This review aims to inspire a new thrust toward the contribution of the FA pathway to drug resistance in cancer. We believe an indepth understanding of this pathway will open new frontiers to effectively treat drug-resistant cancer.

Understanding Cancer Drug Resistance by Developing and Studying Resistant Cell Line Models

2016 ◽  
Vol 16 (3) ◽  
pp. 226-237 ◽  
Author(s):  
Cristina P.R. Xavier ◽  
Milica Pesic ◽  
M. Helena Vasconcelos
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Cancer Drug ◽  
Cancer Drug Resistance
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