Repression of cyclin D1 as a target for germ cell tumors [PDF]
Metastatic germ cell tumors (GCT) are curable, however GCTs refractory to cisplatin-based chemotherapy have a poor prognosis. This study explores D-type cyclins as molecular targets in GCTs because all-trans-retinoic acid (RA)-mediated differentiation of
Bee, Thomas +10 more
core
Cyclin D1 overexpression supports stable EBV infection in nasopharyngeal epithelial cells [PDF]
Undifferentiated nasopharyngeal carcinomas (NPCs) are commonly present with latent EBV infection. However, events regulating EBV infection at early stages of the disease and the role of EBV in disease pathogenesis are largely undefined.
Chen, H +14 more
core +2 more sources
This study identifies a FOSL2‐driven positive feedback loop that amplifies FSH/FSHR signaling. During FSH‐dependent follicle maturation, FSH induces Fosl2 expression via the cAMP‐PKA‐CREB cascade. FOSL2 in turn binds the promoters of Fshr and estrogen‐biosynthesis genes to enhance their transcription, thereby increasing Fshr mRNA level and amplifying ...
Hongru Shi +13 more
wiley +1 more source
The cyclin D1 proto-oncogene is sequestered in the cytoplasm of mammalian cancer cell lines
Background The cyclin D1 proto-oncogene is an important regulator of G1 to S-phase transition and an important cofactor for several transcription factors in numerous cell types. Studies on neonatal cardiomyocytes and postmitotic neurons indicate that the
Coombes R Charles +6 more
doaj +1 more source
In vitro activities of novel 4-HPR derivatives on a panel of rhabdoid and other tumor cell lines [PDF]
Background Rhabdoid tumors (RTs) are aggressive pediatric malignancies with poor prognosis. N-(4-hydroxy phenyl) retinamide (4-HPR or fenretinide) is a potential chemotherapeutic for RTs with activity correlated to its ability to down-modulate Cyclin D1.
Melissa E Smith +2 more
core +2 more sources
SDPR–STK38 axis controls the proliferation–differentiation balance in alveolar type II cells
The present study identifies SDPR as a pivotal regulator orchestrating the balance between proliferation and differentiation in alveolar type II (AT2) cells. In SDPR+/+ cells, SDPR binds to and inhibits STK38 activity, thereby sustaining GSK‐3β signaling functionality to promote cyclin D1 degradation and maintain cell cycle homeostasis.
Jie Wang +6 more
wiley +1 more source
Cyclin D3 deficiency inhibits skin tumor development, but does not affect normal keratinocyte proliferation. [PDF]
Rearrangement and amplification of the D-type cyclin genes have been reported in human cancer. Previous studies have demonstrated that Ras-mediated skin tumorigenesis depends on pathways that act through cyclin D1 and D2; however, the role of cyclin D3 ...
Kim, S.H. +4 more
core +1 more source
Cyclin D1 Functions in Cell Migration [PDF]
Cell migration is essential for developmental morphogenesis, tissue repair, and tumor metastasis. A recent study reveals that cyclin D1 acts to promote cell migration by inhibiting Rho/ROCK signaling and expression of thrombospondin-1 (TSP-1), an extracellular matrix protein that regulates cell migration in many settings including cancer.
Zhiping, Li +3 more
openaire +2 more sources
Therapeutic Applications of Stimuli‐Based Release and Engineering of Extracellular Vesicles
This review summarizes the effects of endogenous and exogenous stimuli, their effects on the natural release of extracellular vesicles, as well as their uptake and release. It also gives an overview of stimuli‐responsive EVs and their therapeutic applications. Extracellular vesicles (EVs), nano‐ to microsized lipid bilayer membrane‐bound particles, are
Gloria Kemunto, Kristen Dellinger
wiley +1 more source
Glycogen synthase kinase 3 has a limited role in cell cycle regulation of cyclin D1 levels
Background The expression level of cyclin D1 plays a vital role in the control of proliferation. This protein is reported to be degraded following phosphorylation by glycogen synthase kinase 3 (GSK3) on Thr-286. We recently showed that phosphorylation of
Hitomi Masahiro +6 more
doaj +1 more source

