Drug resistance and Cancer stem cells

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Abstract

Therapy resistance is a major problem when treating cancer patients as cancer cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones that contribute to poor prognosis. Therapy resistance can be both intrinsic and/or acquired. These are multifactorial events, and some are related to factors including adaptations in cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), deregulation of key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, and activation of DNA damage response among others. Among these factors, CSCs represent the major source of therapy resistance. CSCs are a subset of tumor cells that are capable of self-renewal and multilineage progenitor expansion that are known to be intrinsically resistant to anticancer treatments. Multiple clones of CSCs pre-exist, and some can adopt and expand easily to changes in the tumor microenvironment (TME) and/or in response to radio- and chemotherapy. A combination of both intrinsic and extrinsic factors contributes to CSC-mediated therapy resistance. In this review, we will focus on CSCs and therapy resistance as well as suggest strategies to eliminate CSCs and, therefore, overcome resistance.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12964-020-00627-5.

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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, Ilio Vitale, Stuart A. Aaronson … (2018)

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

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Hippo Pathway in Organ Size Control, Tissue Homeostasis, and Cancer.

Fa-Xing Yu, Bin Zhao, Kun-Liang Guan (2015)

Two decades of studies in multiple model organisms have established the Hippo pathway as a key regulator of organ size and tissue homeostasis. By inhibiting YAP and TAZ transcription co-activators, the Hippo pathway regulates cell proliferation, apoptosis, and stemness in response to a wide range of extracellular and intracellular signals, including cell-cell contact, cell polarity, mechanical cues, ligands of G-protein-coupled receptors, and cellular energy status. Dysregulation of the Hippo pathway exerts a significant impact on cancer development. Further investigation of the functions and regulatory mechanisms of this pathway will help uncovering the mystery of organ size control and identify new targets for cancer treatment.

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Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.

In-kyung Park, Dalong Qian, Mark J. Kiel … (2003)

A central issue in stem cell biology is to understand the mechanisms that regulate the self-renewal of haematopoietic stem cells (HSCs), which are required for haematopoiesis to persist for the lifetime of the animal. We found that adult and fetal mouse and adult human HSCs express the proto-oncogene Bmi-1. The number of HSCs in the fetal liver of Bmi-1-/- mice was normal. In postnatal Bmi-1-/- mice, the number of HSCs was markedly reduced. Transplanted fetal liver and bone marrow cells obtained from Bmi-1-/- mice were able to contribute only transiently to haematopoiesis. There was no detectable self-renewal of adult HSCs, indicating a cell autonomous defect in Bmi-1-/- mice. A gene expression analysis revealed that the expression of stem cell associated genes, cell survival genes, transcription factors, and genes modulating proliferation including p16Ink4a and p19Arf was altered in bone marrow cells of the Bmi-1-/- mice. Expression of p16Ink4a and p19Arf in normal HSCs resulted in proliferative arrest and p53-dependent cell death, respectively. Our results indicate that Bmi-1 is essential for the generation of self-renewing adult HSCs.

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Author and article information

Contributors

Yuan Li: 15942066533@163.com

Zhenning Wang: josieon826@sina.cn

Jaffer A. Ajani: jajani@mdanderson.org

Shumei Song: ssong@mdanderson.org

Journal

Journal ID (nlm-ta): Cell Commun Signal

Journal ID (iso-abbrev): Cell Commun Signal

Title: Cell Communication and Signaling : CCS

Publisher: BioMed Central (London )

ISSN (Electronic): 1478-811X

Publication date (Electronic): 15 February 2021

Publication date PMC-release: 15 February 2021

Publication date Collection: 2021

Volume: 19

Electronic Location Identifier: 19

Affiliations

[1 ]GRID grid.240145.6, ISNI 0000 0001 2291 4776, Department of Gastrointestinal Medical Oncology, , The University of Texas MD Anderson Cancer Center, ; 1515 Holcombe Boulevard, Houston, TX 77030-4009 USA

[2 ]GRID grid.412636.4, Department of Surgical Oncology and General Surgery, , First Hospital of China Medical University, ; Shenyang, 110001 People’s Republic of China

Article

Publisher ID: 627

DOI: 10.1186/s12964-020-00627-5

PMC ID: 7885480

PubMed ID: 33588867

SO-VID: 2b1902b3-98c7-4669-bb06-3008303dec01

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 30 April 2020

Date accepted : 9 July 2020

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100007313, University of Texas MD Anderson Cancer Center;

Award ID: 3-0026317

Award Recipient : Shumei Song

Funded by: the U.S. Department of Defense

Award ID: CA160433

Award Recipient : Shumei Song

Funded by: FundRef http://dx.doi.org/10.13039/100000009, Foundation for the National Institutes of Health;

Award ID: CA129906, CA138671, CA172741

Award Recipient : Jaffer A. Ajani

Custom metadata

ScienceOpen disciplines: Cell biology

Keywords: drug resistance,cancer stem cells,emt and tme

Data availability:

ScienceOpen disciplines: Cell biology

Keywords: drug resistance, cancer stem cells, emt and tme

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