scholarly journals Crucial role of HMGA1 in the self-renewal and drug resistance of ovarian cancer stem cells

2016 ◽  
Vol 48 (8) ◽  
pp. e255-e255 ◽  
Author(s):  
Dae Kyoung Kim ◽  
Eun Jin Seo ◽  
Eun J Choi ◽  
Su In Lee ◽  
Yang Woo Kwon ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Crucial Role ◽  
The Self ◽  
Ovarian Cancer Stem Cells ◽  
Self Renewal

Abstract 2495: hPaf1/PD2 interacts with OCT3/4 in maintenance of the self-renewal process of ovarian cancer stem cells

2016 ◽  
Author(s):  
Saswati Karmakar ◽  
Parthasarathy Seshacharyulu ◽  
Arokia Priyanka Vaz ◽  
Imayavaramban Lakshmanan ◽  
Moorthy Palanimuthu Ponnusamy ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Renewal Process ◽  
The Self ◽  
Ovarian Cancer Stem Cells ◽  
Self Renewal

Abstract 256: Elucidating the role of ARID3B in ovarian cancer stem cells.

2013 ◽  
Author(s):  
Victoria E. Deneke ◽  
Lynn Roy ◽  
Richard Dahl ◽  
Karen D. Cowden Dahl
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Ovarian Cancer Stem Cells

scholarly journals Vitamin D-Induced Molecular Mechanisms to Potentiate Cancer Therapy and to Reverse Drug-Resistance in Cancer Cells

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1798 ◽  
Author(s):  
Mariarosaria Negri ◽  
Annalisa Gentile ◽  
Cristina de Angelis ◽  
Tatiana Montò ◽  
Roberta Patalano ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Vitamin D ◽  
Drug Resistance ◽  
Cancer Therapy ◽  
Cancer Stem Cells ◽  
Crucial Role ◽  
Molecular Mechanisms ◽  
Vitamin D Supplementation

Increasing interest in studying the role of vitamin D in cancer has been provided by the scientific literature during the last years, although mixed results have been reported. Vitamin D deficiency has been largely associated with various types of solid and non-solid human cancers, and the almost ubiquitous expression of vitamin D receptor (VDR) has always led to suppose a crucial role of vitamin D in cancer. However, the association between vitamin D levels and the risk of solid cancers, such as colorectal, prostate and breast cancer, shows several conflicting results that raise questions about the use of vitamin D supplements in cancer patients. Moreover, studies on vitamin D supplementation do not always show improvements in tumor progression and mortality risk, particularly for prostate and breast cancer. Conversely, several molecular studies are in agreement about the role of vitamin D in inhibiting tumor cell proliferation, growth and invasiveness, cell cycle arrest and inflammatory signaling, through which vitamin D may also regulate cancer microenvironment through the activation of different molecular pathways. More recently, a role in the regulation of cancer stem cells proliferation and short non-coding microRNA (miRNAs) expression has emerged, conferring to vitamin D a more crucial role in cancer development and progression. Interestingly, it has been shown that vitamin D is able not only to potentiate the effects of traditional cancer therapy but can even contribute to overcome the molecular mechanisms of drug resistance—often triggering tumor-spreading. At this regard, vitamin D can act at various levels through the regulation of growth of cancer stem cells and the epithelial–mesenchymal transition (EMT), as well as through the modulation of miRNA gene expression. The current review reconsiders epidemiological and molecular literature concerning the role of vitamin D in cancer risk and tumor development and progression, as well as the action of vitamin D supplementation in potentiating the effects of drug therapy and overcoming the mechanisms of resistance often triggered during cancer therapies, by critically addressing strengths and weaknesses of available data from 2010 to 2020.

scholarly journals Inhibiting of self-renewal, migration and invasion of ovarian cancer stem cells by blocking TGF-β pathway

PLoS ONE ◽  
2020 ◽  
Vol 15 (3) ◽  
pp. e0230230
Author(s):  
Haiyan Wen ◽  
Min Qian ◽  
Jing He ◽  
Meihui Li ◽  
Qing Yu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Migration And Invasion ◽  
Ovarian Cancer Stem Cells ◽  
Self Renewal

Superparamagnetic Iron Oxide Nanoparticles Induce Ferroptosis of Human Ovarian Cancer Stem Cells by Weakening Cellular Autophagy

2020 ◽  
Vol 16 (11) ◽  
pp. 1612-1622
Author(s):  
Yongyi Huang ◽  
Jiajia Lin ◽  
Ying Xiong ◽  
Juan Chen ◽  
Xiling Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Superparamagnetic Iron Oxide ◽  
Oxide Nanoparticles ◽  
Human Ovarian Cancer ◽  
Ovarian Cancer Stem Cells

Human ovarian cancer stem cells (HuOCSCs) are the main source of ovarian cancer recurrence, metastasis, and drug resistance. Superparamagnetic iron oxide nanoparticles (SPIONs) are well-known nucleic acid or drug carriers owing to their controllable properties, superior stability, and easy modification. However, whether SPIONs can inhibit the activity of HuOCSCs by inducing ferroptosis remains unclear. In the present study, we isolated CD44+ /CD133+ HuOCSCs from tumours of four patients with clear cell ovarian cancer and added 0.2 mM SPIONs for mixed culture. Transmission electron microscopy showed that SPION-treated HuOCSCs contained multiple high-density electron clouds. Prussian blue staining showed high concentrations of iron ions in the cells. In vitro , SPIONs treatment of HuOCSCs inhibited cell proliferation, migration, and soft agar clone formation, weakened their resistance to multiple chemotherapeutics, and induced cell death. In vivo , SPIONs pretreatment of HuOCSCs significantly reduced their tumour-forming ability and induced angiogenesis in nude mice. Further, SPIONs induced the accumulation of reactive oxygen species in HuOCSCs and induced oxidative stress. qPCR analysis indicated that SPIONs-treated HuOCSCs had reduced expression of tumour stem cell markers (CD117, NANOG, CD133, and SOX2), cell proliferation factors (KI67, CCND), autophagy-related factors (ATG3, ATG5, MAP1ALC3a, MAP1ALC3b, and MAP1ALC3c), and certain negative regulators of ferroptosis, while the mRNA expression levels of cell death-related proteins (BAK1 and BID), and certain positive regulators of ferroptosis were significantly increased. Overall, our findings suggest that SPIONs induce oxidative stress and decrease autophagy activity in ovarian cancer stem cells, activate ferroptosis, and inhibit their proliferation, invasion, drug resistance, and tumorigenic ability.

scholarly journals Role of the Microenvironment in Ovarian Cancer Stem Cell Maintenance

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Jennifer Pasquier ◽  
Arash Rafii
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Biology ◽  
Tumor Stroma ◽  
Cellular Component ◽  
Cytokine Network ◽  
Ovarian Cancer Stem Cells ◽  
Stem Cell Maintenance

Despite recent progresses in cancer therapy and increased knowledge in cancer biology, ovarian cancer remains a challenging condition. Among the latest concepts developed in cancer biology, cancer stem cells and the role of microenvironment in tumor progression seem to be related. Indeed, cancer stem cells have been described in several solid tumors including ovarian cancers. These particular cells have the ability to self-renew and reconstitute a heterogeneous tumor. They are characterized by specific surface markers and display resistance to therapeutic regimens. During development, specific molecular cues from the tumor microenvironment can play a role in maintaining and expanding stemness of cancer cells. The tumor stroma contains several compartments: cellular component, cytokine network, and extracellular matrix. These different compartments interact to form a permissive niche for the cancer stem cells. Understanding the molecular cues underlying this crosstalk will allow the design of new therapeutic regimens targeting the niche. In this paper, we will discuss the mechanisms implicated in the interaction between ovarian cancer stem cells and their microenvironment.

Sign in / Sign up

Export Citation Format

Share Document