Formation of Benign Tumours by Stem Cell Misregulation

Our tissues usually have just the right number of cells to optimally fulfil their function. Not enough cells within a tissue can lead to dysfunction, while too many cells result in a tumour. Yet, how this homeostatic balance is maintained remains poorly defined. Most differentiated cells within tissues have a finite lifespan and need to be replaced at a corresponding pace to maintain tissue homeostasis. These new differentiated cells are generated by proliferation of the stem/progenitor cells that serve the tissue. Work in simple invertebrates clearly suggests stem cells respond to at least two types of signals: niche signaling and growth factors. Niche signals promote the undifferentiated state by preventing differentiation, and thus allow for stem cell self-renewal. Growth factor sources comprise a systemic input reflecting the animal’s nutritional status, and a localized, homeostatic feedback from the tissue that the stem cells serve. That homeostatic signal couples stem cell proliferation rates to the tissue’s need for new differentiated cells. Evidence from simple organisms suggests two types of benign tumours can arise from deregulation of either niche or homeostatic signaling. Namely, constitutive niche signaling promotes the formation of undifferentiated “stem cell” tumours, while defective homeostatic signaling leads to the formation of differentiated tumours. We propose that these principles may be conserved and underlie benign tumour formation in humans, while benign tumours can evolve into cancer.

The Impact of Fasciation on Maize Inflorescence Architecture

How functional genetics research can be applied to improving crop yields is a timely challenge. One of the most direct methods is to produce larger inflorescences with higher productivity, which should be accompanied by a balance between stem cell proliferation and lateral organ initiation in meristems. Unbalanced proliferation of stem cells causes the fasciated inflorescences, which reflect the abnormal proliferation of meristems, derived from the Latin word ‘fascis’, meaning ‘bundle’. Maize, a model system for grain crops, has shown tremendous yield improvements through the mysterious transformation of the female inflorescence during domestication. In this review, we focus on maize inflorescence architecture and highlight the patterns of fasciation, including recent progress.

Osteon-mimetic 3D nanofibrous scaffold enhancing stem cell proliferation and osteogenic differentiation for bone regeneration

Scaffold microstructure is important for bone tissue engineering. Failure to synergistically imitate the hierarchical microstructure of bone component, such as osteon with concentric multilayers assembled by nanofibers, hindered the performance...

Quercetin promotes bone marrow mesenchymal stem cell proliferation and osteogenic differentiation through the H19/miR-625-5p axis to activate the Wnt/β-catenin pathway

Background Quercetin and H19 can promote osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). However, whether quercetin regulates H19 expression to promote osteogenic differentiation of BMSCs is unclear. Methods BMSC proliferation, matrix mineralization, and alkaline phosphatase (ALP) activity were assessed using the Cell Counting Kit-8, ALP assay kit, and alizarin red staining kit, respectively. Expression of H19, miR-625-5p, BMP-2, osteocalcin, and RUNX2 were measured by qRT-PCR; β-catenin protein level was measured by western blotting. Results Quercetin promoted BMSC proliferation, enhanced ALP activity, and upregulated the expression of BMP-2, osteocalcin, and RUNX2 mRNAs, suggesting that it promoted osteogenic differentiation of BMSCs. Moreover, quercetin increased H19 expression, while the effect of quercetin on BMSCs was reversed by silencing H19 expression. Additionally, miR-625-5p, interacted with H19, was downregulated during quercetin-induced BMSC osteogenic differentiation, which negatively correlated with H19 expression. Silencing miR-625-5p expression promoted BMSC proliferation and osteogenic differentiation, whereas miR-625-5p overexpression weakened the effect of quercetin on BMSCs. Finally, quercetin treatment or downregulation of miR-625-5p expression increased β-catenin protein level in BMSCs. Upregulation or downregulation of miR-625-5p or H19 expression, respectively, inhibited β-catenin protein level in quercetin treated-BMSCs. Conclusion H19 promotes, while miR-625-5p inhibits BMSC osteogenic differentiation. Quercetin activates the Wnt/β-catenin pathway and promotes BMSC osteogenic differentiation via the H19/miR-625-5p axis.

Transitions in development – an interview with Rosa Uribe

Rosa Uribe is an Assistant Professor of BioSciences at Rice University. Having established her lab in 2017, her research focusses on identifying the genetic, cellular and signalling-level mechanisms of neural crest stem cell proliferation, migration and differentiation during embryogenesis. We caught up with Rosa to find out more about her career, her opinions about mentorship and a series of virtual seminars that she co-organises.