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Trending Papers in cell biology

Prostaglandin E2 and Cancer: Insight into Tumor Progression and Immunity
Published: Dec 2020
The involvement of inflammation in cancer progression has been the subject of research for many years. Inflammatory milieu and immune response are associated with cancer progression and recurrence. In different types of tumors, growth and metastatic phenotype characterized by the epithelial mesenchymal transition (EMT) process, stemness, and angiogenesis, are increasingly associated with intrinsic or extrinsic inflammation. Among the inflammatory mediators, prostaglandin E2 (PGE2) supports epithelial tumor aggressiveness by several mechanisms, including growth promotion, escape from apoptosis, transactivation of tyrosine kinase growth factor receptors, and induction of angiogenesis. Moreover, PGE2 is an important player in the tumor microenvironment, where it suppresses antitumor immunity and regulates tumor immune evasion, leading to increased tumoral progression. In this review, we describe the current knowledge on the pro-tumoral activity of PGE2 focusing on its role in cancer progression and in the regulation of the tumor microenvironment.
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In stem cells the cell cycle length of early divisions influences the cell cycle length of later divisions
From Paper: Cell cycle lengths of stem cells and their lineage from cellular demography
Published: Nov 2020
  • Dynamic regulation of the proliferation rate of stem cells and their transit-amplifying daughters maintains tissue homeostasis in different conditions such as tissue regeneration, aging, and hormonal imbalance. Previous studies suggested that a molecular clock in the stem cell progeny determines the timing of differentiation.
Treatment of breast cancer by targeting mitochondria
From Paper: Treatment of ErbB2 breast cancer by mitochondrial targeting
Published: Jul 2020
  • MEDICA treatment is shown here to suppress ErbB2 breast tumors and lung metastasis in transgenic mice that express the activated ErbB2/neu oncogene under the control of the mouse MMTV long terminal repeat (LTR) promoter
  • Suppression of ErbB2 breast tumors by MEDICA in ErbB2/neu mouse transgenes as well as in human ErbB2 breast cancer cells was accompanied by loss of plasma membrane ErbB2, together with other ErbB family members, including EGFR (ErbB1) and ErbB3
In plants DNA damage triggers reprogramming into stem cells
Published: Aug 2020
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  • These findings indicate that DNA strand breaks, which are usually considered to pose a severe threat to cells, trigger cellular reprogramming towards stem cells via the activity of ATR and STEMINs
Arc Gene Acts Like a Virus to Pass mRNA from Neuron to Neuron
  • The genetic material, messenger RNA (mRNA) from the Arc gene, can be passed from neuron to neuron.
A universal trade-off between growth and lag in fluctuating environments
  • There is a trade-off between steady-state growth rate and physiological adaptability in Escherichia coli.
  • A model of sequential flux limitation not only explains the observed trade-off between growth and adaptability, but also allows quantitative predictions regarding the universal occurrence of such tradeoffs, based on the opposing enzyme requirements of glycolysis versus gluconeogenesis.
Auxin-induced signaling protein nanoclustering contributes to cell polarity formation
Published: Aug 2020
  • This study propose a new paradigm for polarity formation: A diffusive signal triggers cell polarization by promoting cell surface receptor-mediated nanoclustering of signaling components and cytoskeleton-mediated positive feedback that reinforces these nanodomains into polarized domains.
  • Phytohormone auxin-induced, sterol-dependent nanoclustering of cell surface transmembrane receptor kinase 1 (TMK1) is critical for the formation of polarized domains at the plasma membrane (PM) during the morphogenesis of cotyledon pavement cells (PC) in Arabidopsis.
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Transplantation of muscle stem cell mitochondria rejuvenates the bioenergetic function of dystrophic muscle
Mohiuddin, Mahir, et al
Published: Apr 2020
Mitochondrial dysfunction has been implicated in various pathologies, including muscular dystrophies. During muscle regeneration, resident stem cells, also known as muscle satellite cells (MuSCs), undergo myogenic differentiation to form de novo myofibers or fuse to existing syncytia. Leveraging this cell-cell fusion process, we postulated that mitochondria stemming from MuSCs could be transferred to myofibers during muscle regeneration to remodel the mitochondrial network and restore bioenergetic function. Here, we report that dystrophic MuSCs manifest significant mitochondrial dysfunction and fuse with existing dystrophic myofibers to propagate mitochondrial dysfunction during muscle repair. We demonstrate that by transplanting healthy donor MuSCs into dystrophic host muscle, the mitochondrial network (reticulum) and bioenergetic function can be rejuvenated. Conversely, when bioenergetically-compromised donor MuSCs are transplanted, improvements in mitochondrial organization and bioenergetic function were ablated in the dystrophic recipient. Overall, these data reveal a unique role of muscle stem cells as an essential regulator of myofiber mitochondrial homeostasis and a potential therapeutic target against mitochondrial myopathies.### Competing Interest StatementThe authors have declared no competing interest.
Retrieved from biorxiv
Complementary α-arrestin - Rsp5 ubiquitin ligase complexes control selective nutrient transporter endocytosis in response to amino acid availability
Ivashov, Vasyl, et al
Published: Apr 2020
How cells adjust transport across their membranes is incompletely understood. Previously, we have shown that S.cerevisiae broadly re-configures the nutrient transporters at the plasma membrane in response to amino acid availability, through selective endocytosis of sugar- and amino acid transporters (AATs) (Mueller et al., 2015). A genome-wide screen now revealed that Art2/Ecm21, a member of the α-arrestin family of Rsp5 ubiquitin ligase adaptors, is required for the simultaneous endocytosis of four AATs and induced during starvation by the general amino acid control pathway. Art2 uses a basic patch to recognize C-terminal acidic sorting motifs in these AATs and instructs Rsp5 to ubiquitinate proximal lysine residues. In response to amino acid excess, Rsp5 instead uses TORC1-activated Art1 to detect N-terminal acidic sorting motifs within the same AATs, which initiates exclusive substrate-induced endocytosis of individual AATs. Thus, amino acid availability activates complementary α-arrestin-Rsp5-complexes to control selective endocytosis for nutrient acquisition.### Competing Interest StatementThe authors have declared no competing interest.
Retrieved from biorxiv
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