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Identification and expansion of human colon-cancer-initiating cells
TLDR
It is concluded that colorectal cancer is created and propagated by a small number of undifferentiated tumorigenic CD133+ cells, which should therefore be the target of future therapies.
MicroRNA-133 controls cardiac hypertrophy
TLDR
The data show thatmiR-133, and possibly miR-1, are key regulators of cardiac hypertrophy, suggesting their therapeutic application in heart disease.
Identification and expansion of the tumorigenic lung cancer stem cell population
TLDR
Lung cancer contains a rare population of CD133+ cancer stem-like cells able to self-renew and generates an unlimited progeny of non-tumorigenic cells, which may provide valuable information to be exploited in the clinical setting.
The miR-15a–miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities
TLDR
It is proposed thatmiR-15a and miR-16 act as tumor suppressor genes in prostate cancer through the control of cell survival, proliferation and invasion through the regulation of BCL2 and CCND1.
Antagomir-17-5p Abolishes the Growth of Therapy-Resistant Neuroblastoma through p21 and BIM
TLDR
In vitro or in vivo treatment with antagomir-17-5p abolishes the growth of MYCN-amplified and therapy-resistant neuroblastoma through p21 and BIM upmodulation, leading to cell cycling blockade and activation of apoptosis, respectively.
Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha.
TLDR
The capacity of human astrocytes to synthesize and release cytokines active on hemolymphopoietic cells supports the concept that these cells play an important role in the regulation of inflammatory and immune responses in a variety of brain pathologies.
MicroRNAs 17-5p–20a–106a control monocytopoiesis through AML1 targeting and M-CSF receptor upregulation
TLDR
These studies indicate that monocytopoiesis is controlled by a circuitry involving sequentially miRNA 17-5p–20a–106a, AML1 and M-CSFR, whereby miRNAs function as a master gene complex interlinked withAML1 in a mutual negative feedback loop.
A three-step pathway comprising PLZF/miR-146a/CXCR4 controls megakaryopoiesis
TLDR
The data indicate that megakaryopoiesis is controlled by a cascade pathway, in which PLZF suppresses miR-146a transcription and thereby activates CXCR4 translation.
MicroRNAs 221 and 222 inhibit normal erythropoiesis and erythroleukemic cell growth via kit receptor down-modulation.
TLDR
It is indicated that the decline of miR 221 and 222 during exponential E growth unblocks kit protein production at mRNA level, thus leading to expansion of early erythroblasts, and the results on kit+ erythroleukemic cells suggest a potential role of these miRs in cancer therapy.
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