517 DYNAMIC OF GENE EXPRESSION OF STEM CELL MARKERS DURING INVASIVE GROWTH OF PROSTATE CANCER CELLS

The proliferation-quiescence decision is a dynamic process that remains incompletely understood. Live-cell imaging with fluorescent cell cycle sensors now allows us to visualize the dynamics of cell cycle transitions and has revealed that proliferation-quiescence decisions can be highly heterogeneous, even among clonal cell lines in culture. Under normal culture conditions, cells often spontaneously enter non-cycling G0 states of varying duration and depth. This also occurs in cancer cells and G0 entry in tumors may underlie tumor dormancy and issues with cancer recurrence. Here we show that a cell cycle indicator previously shown to indicate G0 upon serum starvation, mVenus-p27K-, can also be used to monitor spontaneous quiescence in untransformed and cancer cell lines. We find that the duration of spontaneous quiescence in untransformed and cancer cells is heterogeneous and that a portion of this heterogeneity results from asynchronous proliferation-quiescence decisions in pairs of daughters after mitosis, where one daughter cell enters or remains in temporary quiescence while the other does not. We find that cancer dormancy signals influence both entry into quiescence and asynchronous proliferation-quiescence decisions after mitosis. Finally, we show that spontaneously quiescent prostate cancer cells exhibit altered expression of components of the Hippo pathway and are enriched for the stem cell markers CD133 and CD44. This suggests a hypothesis that dormancy signals could promote cancer recurrence by increasing the proportion of quiescent tumor cells poised for cell cycle re-entry with stem cell characteristics in cancer.

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Lutein Regulates the Expression of Apoptosis-related Genes and Stem Cell Markers in A549 Human Lung Cancer Cells

Natural Product Communications ◽

10.1177/1934578x1701200616 ◽

2017 ◽

Vol 12 (6) ◽

pp. 1934578X1701200 ◽

Cited By ~ 1

Author(s):

Kazuo Yamagata ◽

Ayame Fujiwara ◽

Daiki Onodera ◽

Tagami Motoki

Keyword(s):

Gene Expression ◽

Lung Cancer ◽

Stem Cell ◽

Cancer Cells ◽

Human Lung ◽

Stem Cell Marker ◽

Human Lung Cancer ◽

Stem Cell Markers ◽

Cell Markers ◽

Bcl2 Family

The BCL2 family has both pro-apoptotic and anti-apoptotic functions. Furthermore, stem cell markers such as Oct4, SOX2, and NANOG enhance cancer cells’ self-renewal, resistance to anti-cancer drugs and clonal growth. Therefore, selective inhibition of BCL2 genes and downregulated expression of stem cell markers should reduce the survival of cancer cells. Previous studies have reported that lutein, a carotenoid pigment present in fruits and vegetables, can inhibit cancer cells. However, the inhibitory effects of lutein on cancer cells have not been investigated sufficiently. In this study, we used gene expression analysis by polymerase chain reaction (PCR) and Western blotting to show that lutein regulates the expression of genes involved in apoptosis and several stem cell marker genes in a human lung cancer cell line, A549. Lutein induced gene expression of pro-apoptotic BAX and CAS3 and reduced the level of the anti-apoptotic gene BCL2. Furthermore, protein expression of BCL2 and BAX was regulated by treatment with lutein. Lutein also inhibited SOX2 and NANOG gene expression in A549, but not POU5F1. In addition, lutein reduced gene expression of SLCA11, but induced CD44 and CD133 gene expression. These results indicated that lutein inhibits several events associated with apoptosis regulation in a BCL2 family-dependent pathway.

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The Significance of Cancer Stem Cell Markers’ Gene Expression and Relevance for Survival Outcomes

10.20944/preprints202005.0047.v1 ◽

2020 ◽

Cited By ~ 1

Author(s):

Kevin Dzobo ◽

Dimakatso Senthebane ◽

Chelene Ganz ◽

Nicholas Thomford

Keyword(s):

Gene Expression ◽

Stem Cell ◽

Cancer Stem Cell ◽

Cancer Cells ◽

Therapy Resistance ◽

Stem Cell Markers ◽

Cancer Drugs ◽

Cell Markers ◽

Cancer Stem Cell Markers ◽

New Findings

Solid tumors display complex biology and most therapies including chemotherapy cannot prevent therapy resistance and relapse. Most therapeutics target cancer cells, but recent data suggest the presence of cancer stem cells as cells with self-renewal and tumorigenic abilities. Cancer stem cell markers have been suggested to have prognostic value and can be targeted during cancer treatment and in resistant disease. CSCs have been postulated to play significant contextual roles in tumor initiation, progression, therapy resistance and metastasis. CSCs have thus been targeted by new generation cancer drugs. The transcriptional expression of several CSC markers in different cancers was evaluated by searching publicly available The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) databases. We report here new findings on expression and prognostic significance of CSC markers in several cancers by examining the expression of CSCs markers in tumor tissues versus the adjacent normal tissues. We found that CSC markers were mostly highly expressed various tumors such as colon, lung, pancreatic and esophageal cancers. No CSC marker is expressed in the same pattern in all cancers and individual CSC marker expression was not linked to patient survival. This analysis calls for continued research on CSCs and clinical evaluation of the CSC markers in relation to prognosis of cancers in large population samples. Novel cancer drugs ought to target CSCs, cancer cells and tumor microenvironment variations.

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