About This Journal

An open access home for your cell proliferation research

Cell Proliferation is an open access journal devoted to studies into all aspects of cell proliferation and differentiation in normal and abnormal states.

Why publish in Cell Proliferation?

  • Open access means your work will be accessible by everyone, resulting in more downloads, increased cites and greater visibility.
  • Receive a fast first decision within just 5 days from submission (median)
  • Discoverable and widely distributed with indexing across EBSCO, Embase, PubMed, Science Citation Index, BIOSIS and more!
  • Dedicated thematic collections make research in specific areas easy to find.

 

Topics include control systems and mechanisms operating at inter- and intracellular, molecular and genetic levels; modification by and interactions with chemical and physical agents; mathematical modelling; and the development of new techniques.

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Articles

ORIGINAL ARTICLE
Open access

DNASE1L3 inhibits proliferation, invasion and metastasis of hepatocellular carcinoma by interacting with β-catenin to promote its ubiquitin degradation pathway

  •  24 June 2022

Abstract

Description unavailable

Decreased expression of DNASE1L3 is associated with poor prognosis in patients with HCC

DNASE1L3 inhibits the proliferation and cell cycle of HCC cells in vitro and promotes the invasion and metastasis of HCC cells

DNASE1L3 inhibits the tumorigenicity and metastasis of HCC cells in vivo

DNASE1L3 interacts with β-catenin and promotes its binding to the β-catenin destroying complex

DNASE1L3 interacts with P21 and stabilizes P21 by mediating the deubiquitin activity

REVIEW
Open access

The modulatory effect of high salt on immune cells and related diseases

  •  23 June 2022

Abstract

Description unavailable

This review describes the modulatory effect of high salt on various immune cells and immune-regulated diseases. High salt significantly affects the differentiation, activation and function of multiple innate and adaptive immune cells and dominantly induces a pro-inflammatory state in microenvironments, thus influencing the development of various immune-regulated diseases and serving as a target or potential therapeutic agent in different disease contexts.

ORIGINAL ARTICLE
Open access

Nivalenol affects Cyclin B1 level and activates SAC for cell cycle progression in mouse oocyte meiosis

  •  23 June 2022

Abstract

Description unavailable

The image showed that NIV exposure caused the microtubule instability, which disrupted the kinetochore-microtubule attachment, and further activated spindle assembly checkpoint in mouse oocytes. Green, α-tubulin; Blue, DNA.

REVIEW
Open access

Novel insights into the interaction between N6-methyladenosine methylation and noncoding RNAs in musculoskeletal disorders

  •  23 June 2022

Abstract

Description unavailable

m6A regulates the expression and function of ncRNAs (i.e., miRNAs, lncRNAs and circRNAs), ncRNAs can also affect m6A-related protein. m6A-related proteins in ncRNA are abnormally expressed and closely associated with bone osteogenic, osteoclastogenic processes and myogenesis, participating in modulating the homoeostasis of skeletal muscle, bone and cartilage. ncRNA m6A modification regulates the pathological and physiological processes of musculoskeletal disorders (i.e., IDD, OP, OS and OA). In IDD, ncRNA m6A modification regulated NP cells glucose metabolism, senescence and pyroptosis. In OP, ncRNA m6A modification regulated BMSCs osteogenic differentiation, osteoblast proliferation, differentiation and bone formation. In OS, ncRNA m6A modification regulated OS cells growth, migration, proliferation and apoptosis. In OA, ncRNA m6A modification regulated chondrocyte apoptosis and ECM degradation.

ORIGINAL ARTICLE
Open access

Triptolide promotes autophagy to inhibit mesangial cell proliferation in IgA nephropathy via the CARD9/p38 MAPK pathway

  •  22 June 2022

Abstract

Description unavailable

The proliferation of glomerular mesangial cells is the most basic pathological feature for IgA nephropathy (IgAN). Galactose-deficient IgA1 (Gd-IgA1) immune complex deposition activates mesangial cells to mediate specific intracellular signal transduction, promotes mesangial cell proliferation, and initiates kidney damage. Autophagy is involved in mesangial cell proliferation. CARD9 is a risk gene for IgAN. The triptolide (TP), purified from Tripterygium wilfordii hook F., promotes autophagy to inhibit mesangial cell proliferation in IgAN via the CARD9/p38 MAPK pathway.

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