Tumor stem cells

Kopper, László; Hajdú, Melinda

doi:10.1007/bf02893458

Cited by 49 publications

(38 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This may be due to the overexpression of stem cell genes, ABC transporters and a reduction in apoptosis. Studies have established that the ABCG2 transporter protein expressed by SP cells is involved in chemotherapy resistance (25,26). In the present study, the percentage of SP cells was reduced to 0.7% following treatment with verapamil.…”

Section: Discussionsupporting

confidence: 50%

Significance of ATP-binding cassette transporter proteins in multidrug resistance of head and neck squamous cell carcinoma

et al. 2015

View full text Add to dashboard Cite

Abstract. According to the cancer stem cell theory, a small subpopulation of cancer cells, known as cancer stem cells (CSCs), exist that are self-renewing and are involved in tumor invasion, metastasis and recurrence. A number of studies have reported that certain cancer cells are able to efflux the Hoechst 33342 dye. These cells are termed side population (SP) cells and share characteristic features of CSCs. The results of the present study revealed that 2.7% of primary head and neck squamous cell carcinoma (HNSCC) cells were SP cells. This was reduced to 0.7% following treatment with verapamil. The immunofluorescence and reverse transcription polymerase chain reaction analysis revealed that SP cells have an enhanced expression of the ATP-binding cassette (ABC) transporter protein ABC subfamily G, member 2 (ABCG2), which has been identified to be actively involved in drug exclusion. Similarly, the mRNA level of the oncogene B lymphoma Mo-MLV insertion region-1 and the stem cell surface proteins nestin and octamer-binding transcription factor-4 were highly expressed in the SP cells compared with the non-SP cells. In addition, it was demonstrated that HNSCC SP cells exhibited increased proliferation and were highly resistant to multiple drugs. These findings suggest that the presence of CSCs, such as SP cells, may be responsible for chemotherapy failure and tumor relapse in patients with HNSCC. Therefore, the identification of a novel therapeutic drug that could effectively target CSCs may help to eradicate refractory tumors.

show abstract

Section: Discussionsupporting

confidence: 50%

Significance of ATP-binding cassette transporter proteins in multidrug resistance of head and neck squamous cell carcinoma

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Furthermore, an emerging concept about cancer stem cells, which have self-renewal ability to perpetuate the disease, has been reported (Kopper and Hajdu, 2004;Cox et al, 2007): the imbalance in the network, involving p16…”

Section: The P16mentioning

confidence: 99%

Cyclin-dependent kinase 1 expression is inhibited by p16INK4a at the post-transcriptional level through the microRNA pathway

Domenech

Catallo

et al. 2010

Oncogene

View full text Add to dashboard Cite

The p16INK4a protein regulates cell cycle progression mainly by inhibiting the activity of G1-phase cyclin-dependent kinases (CDKs) 4 and 6, the subsequent retinoblastoma protein (pRb) phosphorylation and E2F transcription factor release. The p16INK4a protein can also repress the activity of other transcription factors, such as c-myc, nuclear factorkappaB and c-Jun/AP1. Here, we report that, in two p16WT and p53 WT cell lines (MCF7 and U87), p16INK4a overexpression induces a dramatic decrease in CDK1 protein expression. In response to p16 INK4a, the decreased rate of CDK1 protein synthesis, its unchanged protein half-life, unreduced CDK1 mRNA steady-state levels and mRNA half-life allow us to hypothesize that p16INK4a could regulate CDK1 expression at the post-transcriptional level. This CDK1 downregulation is mediated by the 3 0 -untranslated region (3 0 UTR) of CDK1 mRNA as shown by translational inhibition in luciferase assays and is associated with a modified expression balance of microRNAs (miRNAs) that potentially regulate CDK1, analyzed by TaqMan Human microRNA Array. The p16 INK4a-induced expression of two miRNAs (miR-410 and miR-650 chosen as an example) in MCF7 cells is confirmed by individual reverse transcriptionqPCR. Furthermore, we show the interaction of miR-410 or miR-650 with CDK1-3 0 UTR by luciferase assays. Endogenous CDK1 expression decreases upon both miRNA overexpression and increases with their simultaneous inhibition. The induction of miR-410, but not miR-650 could be related to the pRb/E2F pathway. These results demonstrate the post-transcriptional inhibition of CDK1 by p16 INK4a . We suggest that p16INK4a may regulate gene expression by modifying the functional equilibrium of transcription factors and consequently the expression balance of miRNAs.

show abstract

“…Embryonic genes are important in regulating asymmetric cell division, pluripotentiality and/or in maintaining cellular and tissue-specific niches that are necessary for stem cell survival (Kopper and Hajdu, 2004;Ohlstein et al, 2004;Sell, 2004). Genetic mutations within stem cells or alterations in signaling pathways within the stem cell niche are almost certainly central to the early appearance of premalignant cells.…”

Section: Introductionmentioning

confidence: 99%

Cripto-1: a multifunctional modulator during embryogenesis and oncogenesis

et al. 2005

View full text Add to dashboard Cite

It is increasingly evident that genes known to perform critical roles during early embryogenesis, particularly during stem cell renewal, pluripotentiality and survival, are also expressed during the development of cancer. In this regard, oncogenesis may be considered as the recapitulation of embryogenesis in an inappropriate temporal and spatial manner. The epidermal growth factor-Cripto-1/FRL1/cryptic family of proteins consists of extracellular and cell-associated proteins that have been identified in several vertebrate species. During early embryogenesis, epidermal growth factor-Cripto-1/FRL1/ cryptic proteins perform an obligatory role as coreceptors for the transforming growth factor-beta subfamily of proteins, which includes Nodal. Cripto-1 has also been shown to function as a ligand through a Nodal/Alk4-independent signaling pathway that involves binding to glypican-1 and the subsequent activation through src of phosphoinositol-3 kinase/Akt and ras/mitogen-activated protein kinase intracellular pathways. Expression of Cripto-1 is increased in several human cancers and its overexpression is associated with the development of mammary tumors in mice. Here, we review the role of Cripto-1 during embryogenesis, cell migration, invasion and angiogenesis and how these activities may relate to cellular transformation and tumorigenesis. We also briefly discuss evidence suggesting that Cripto-1 may be involved in stem cell maintenance.

show abstract

Tumor stem cells

Cited by 49 publications

References 30 publications

Significance of ATP-binding cassette transporter proteins in multidrug resistance of head and neck squamous cell carcinoma

Significance of ATP-binding cassette transporter proteins in multidrug resistance of head and neck squamous cell carcinoma

Cyclin-dependent kinase 1 expression is inhibited by p16INK4a at the post-transcriptional level through the microRNA pathway

Cripto-1: a multifunctional modulator during embryogenesis and oncogenesis

Contact Info

Product

Resources

About