The epigenetic/noncoding origin of tumor dormancy

Crea, Francesco; Saidy, Nur Ridzwan Nur; Collins, Colin C.; Wang, Yuzhuo

doi:10.1016/j.molmed.2015.02.005

Cited by 65 publications

(57 citation statements)

References 67 publications

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“…Based on the literature data, neoplastic dormancy can be achieved by two distinct ways: either each cancer cell arrests its cell cycle or the whole neoplasm exhibits balanced growth/cell death rates [24]. In order to verify the fact that observed growth arrest of RPMI 8226 cells is not a consequence of increased cell death occurrence in the cocultures, which simply balance the growth of the cell population, we assessed the apoptotic and necrotic cell numbers in individual cell cultures.…”

Section: Resultsmentioning

confidence: 99%

Inflammatory environment created by fibroblast aggregates induces growth arrest and phenotypic shift of human myeloma cells

K¹,

I²,

Mistrík³

et al. 2015

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Multiple myeloma (MM) is characterized by accumulation of clonal plasma cells (PCs) predominantly in the bone marrow but tumor cells appear in the circulation in significant numbers as the disease progress. The occurrence of circulating multiple myeloma cells raises question concerning interactions between these cells and stroma of peripheral organs specifically under certain pathophysiological conditions, e.g., inflammation. Therefore, in the present study we exposed three human multiple myeloma cell lines to sterile inflammation produced in a culture dish by clusters of cell-cell contact-activated dermal fibroblasts. We now observed that myeloma cells responded differently to this particular type of stromal cell activation, nemosis. Two cell lines U-266 and LP-1 were minimally affected by the proinflammatory signalling, while the third cell line RPMI 8226 responded with growth arrest and altered expression of three phenotypic markers CD38, CD45, and CD138, indicating dedifferentiation shift of these cells to less mature PC-like phenotype. In a preliminary study we identified a subclone of cells having similar phenotype in 14 out of 23 analysed specimens of MM patients. This set of data indicates that the observed phenomenon might be clinically relevant. Our results emphasize the potential role of activated stromal fibroblasts and subsequent inflammation in altering phenotype of PCs and directing myeloma progression towards dormancy. Given the significant implication of dormant myeloma cells that might serve as a major cellular basis for the relapse, understanding their unique biology and precise elucidation of the underlying molecular mechanisms for the maintenance of quiescence is important. Therefore, we consider this study as a particular contribution to development of experimental model for in vitro studies of cancer dormancy.

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Section: Resultsmentioning

confidence: 99%

Inflammatory environment created by fibroblast aggregates induces growth arrest and phenotypic shift of human myeloma cells

K¹,

I²,

Mistrík³

et al. 2015

neo

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“…The peculiar feature of tumors is their excessive and uncoordinated growth, which relies on the fact that cancer cells often carry somatic mutations or amplification of specific, growth-related genes or inactivation of tumor suppressor genes. The altered expression of growth-related (or growth suppressor) gene can also be caused by epigenetic mechanisms (Berdasco and Esteller, 2010;Crea et al, 2015;Ouadid-Ahidouch et al, 2015). In the last decade, the molecular knowledge of specific cancers has greatly grown, hence leading to an increasing use of targeted therapies, i.e.…”

Section: Targeting Ion Channels In Oncology: Pros and Consmentioning

confidence: 99%

Novel perspectives in cancer therapy: Targeting ion channels

Arcangeli

Becchetti

2015

Drug Resistance Updates

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“…We have previously proposed that an epigenetic-noncoding interactome may be responsible for the plasticity of dormant cancer cells 8, 9 . In a highly inter-connected network, long non-coding RNAs, microRNAs (miRNAs), and epigenetic effectors orchestrate key cellular functions to facilitate the stochastic needs of neoplastic cells.…”

Section: Introductionmentioning

confidence: 99%

miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer

Nabavi

Saidy

Venalainen

et al. 2017

Sci Rep

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Carcinoma of the prostate is the most common cancer in men. Treatment of aggressive prostate cancer involves a regiment of radical prostectomy, radiation therapy, chemotherapy and hormonal therapy. Despite significant improvements in the last decade, the treatment of prostate cancer remains unsatisfactory, because a significant fraction of prostate cancers develop resistance to multiple treatments and become incurable. This prompts an urgent need to investigate the molecular mechanisms underlying the evolution of therapy-induced resistance of prostate cancer either in the form of castration-resistant prostate cancer (CRPC) or transdifferentiated neuroendocrine prostate cancer (NEPC). By analyzing micro-RNA expression profiles in a set of patient-derived prostate cancer xenograft tumor lines, we identified miR-100-5p as one of the key molecular components in the initiation and evolution of androgen ablation therapy resistance in prostate cancer. In vitro results showed that miR-100-5p is required for hormone-independent survival and proliferation of prostate cancer cells post androgen ablation. In Silico target predictions revealed that miR-100-5p target genes are involved in key aspects of cancer progression, and are associated with clinical outcome. Our results suggest that mir-100-5p is a possible therapeutic target involved in prostate cancer progression and relapse post androgen ablation therapy.

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The epigenetic/noncoding origin of tumor dormancy

Cited by 65 publications

References 67 publications

Inflammatory environment created by fibroblast aggregates induces growth arrest and phenotypic shift of human myeloma cells

Inflammatory environment created by fibroblast aggregates induces growth arrest and phenotypic shift of human myeloma cells

Novel perspectives in cancer therapy: Targeting ion channels

miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer

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