Book ChapterDOI
The Role of Cancer Stem Cells in Recurrent and Drug-Resistant Lung Cancer.
TLDR
The potential role of the natural agents and synthetic derivatives of natural compounds with anti-cancer activity, e.g. curcumin, CDF, and BR-DIM is highlighted in overcoming therapeutic resistance, suggesting that the above mentioned agents could be important for better treatment of lung cancer in combination therapy.Abstract:
Lung cancer is the leading cause of cancer-related deaths worldwide with a 5-year overall survival rate of less than 20 %. Considering the treatments currently available, this statistics is shocking. A possible explanation for the disconnect between sophisticated treatments and the survival rate can be related to the post-treatment enrichment of Cancer Stem Cells (CSCs), which is one of a sub-set of drug resistant tumor cells with abilities of self-renewal, cancer initiation, and further maintenance of tumors. Lung CSCs have been associated with resistance to radiation and chemotherapeutic treatments. CSCs have also been implicated in tumor recurrence because CSCs are not typically killed after conventional therapy. Investigation of CSCs in determining their role in tumor recurrence and drug-resistance relied heavily on the use of specific markers present in CSCs, including CD133, ALDH, ABCG2, and Nanog. Yet another cell type that is also associated with increased resistance to treatment is epithelial-to-mesenchymal transition (EMT) phenotypic cells. Through the processes of EMT, epithelial cells lose their epithelial phenotype and gain mesenchymal properties, rendering EMT phenotypic cells acquire drug-resistance. In this chapter, we will further discuss the role of microRNAs (miRNAs) especially because miRNA-based therapies are becoming attractive target with respect to therapeutic resistance and CSCs. Finally, the potential role of the natural agents and synthetic derivatives of natural compounds with anti-cancer activity, e.g. curcumin, CDF, and BR-DIM is highlighted in overcoming therapeutic resistance, suggesting that the above mentioned agents could be important for better treatment of lung cancer in combination therapy.read more
Citations
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Journal ArticleDOI
Targeting Cancer Stem Cells: A Strategy for Effective Eradication of Cancer.
TL;DR: The therapeutic strategies for targeting CSCs in several cancers are summarized and the potential and challenges of the approach are discussed.
Journal ArticleDOI
Resistance to Cell Death and Its Modulation in Cancer Stem Cells.
TL;DR: A review article expands on the CSC hypothesis and paradigm with respect to major signaling pathways and effectors that regulate CSC apoptosis resistance and their therapeutic potential for making tumors more responsive to therapy.
Journal ArticleDOI
Cisplatin-enriching cancer stem cells confer multidrug resistance in non-small cell lung cancer via enhancing TRIB1/HDAC activity.
Lihui Wang,Xing Liu,Yong Ren,Jingyuan Zhang,Junli Chen,Wenlong Zhou,Wei Guo,Xiaoxuan Wang,Huiping Chen,Meng Li,Xiangzhong Yuan,Xun Zhang,Jingyu Yang,Chunfu Wu +13 more
TL;DR: Cisplatin, but not paclitaxel and doxorubicin, induced the enrichment of cancer stem cell (CSC) and conferred multidrug resistance in NSCLC cell lines and provided a novel perspective in the evolution of chemotherapy resistance.
Journal ArticleDOI
Targeting autophagy in cancer stem cells as an anticancer therapy.
TL;DR: The recent advances in CSCs and autophagy are reviewed, especially the complex relationship between them are analyzed, and it is hoped that new knowledge will be applied to the strategies for anticancer therapy.
Journal ArticleDOI
Lung cancer stem cells: origin, features, maintenance mechanisms and therapeutic targeting
TL;DR: This review will critically address the CSC concept in lung cancer and its advancement thus far, and highlight some examples on how lung CSCs attain stemness through different molecular modifications and cellular assistance from the tumor microenvironment.
References
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Journal ArticleDOI
The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells
Sendurai A. Mani,Wenjun Guo,Mai Jing Liao,Elinor Ng Eaton,Ayyakkannu Ayyanan,Alicia Y. Zhou,Mary W. Brooks,Ferenc Reinhard,Cheng Cheng Zhang,Michail Shipitsin,Lauren L. Campbell,Kornelia Polyak,Cathrin Brisken,Jing Yang,Robert A. Weinberg +14 more
TL;DR: It is reported that the induction of an EMT in immortalized human mammary epithelial cells (HMLEs) results in the acquisition of mesenchymal traits and in the expression of stem-cell markers, and it is shown that those cells have an increased ability to form mammospheres, a property associated with mammARY epithelial stem cells.
Journal ArticleDOI
Glioma stem cells promote radioresistance by preferential activation of the DNA damage response
Shideng Bao,Qiulian Wu,Roger E. McLendon,Yueling Hao,Qing Ming Shi,Anita B. Hjelmeland,Mark W. Dewhirst,Darell D. Bigner,Jeremy N. Rich +8 more
TL;DR: This work shows that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity, and suggests that CD133-positive tumour cells could be the source of tumour recurrence after radiation.
Journal ArticleDOI
MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Jeffrey A. Engelman,Kreshnik Zejnullahu,Tetsuya Mitsudomi,Youngchul Song,Courtney Hyland,Joon Oh Park,Neal I. Lindeman,Christopher-Michael Gale,Xiaojun Zhao,James J. Christensen,Takayuki Kosaka,Alison J. Holmes,Andrew M. Rogers,Federico Cappuzzo,Tony Mok,Charles Lee,Bruce E. Johnson,Lewis C. Cantley,Pasi A. Jänne +18 more
TL;DR: It is proposed that MET amplification may promote drug resistance in other ERBB-driven cancers as well after it was found that amplification of MET causes gefitinib resistance by driving ERBB3 (HER3)–dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors.
Journal ArticleDOI
Reduced Expression of the let-7 MicroRNAs in Human Lung Cancers in Association with Shortened Postoperative Survival
Junichi Takamizawa,Hiroyuki Konishi,Kiyoshi Yanagisawa,Shuta Tomida,Hirotaka Osada,Hideki Endoh,Tomoko Harano,Yasushi Yatabe,Masato Nagino,Yuji Nimura,Tetsuya Mitsudomi,Takashi Takahashi +11 more
TL;DR: Reduced expression of let-7 in A549 lung adenocarcinoma cell line inhibited lung cancer cell growth in vitro and represents the first report of reduced expression ofLet-7 and the potential clinical and biological effects of such a microRNA alteration.
Journal ArticleDOI
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer
TL;DR: This review will provide potential mechanistic explanations for the association between EMT induction and the emergence of CSCs, and highlight recent studies implicating the function of TGF-β-regulated noncoding RNAs in driving EMT and promoting CSC self-renewal.