Erratum to: Cyclin D1 cooperates with p21 to regulate TGFβ-mediated breast cancer cell migration and tumor local invasion

Dai, Meiou; Al-Odaini, Amal A.; Fils-Aimé, Nadège; Villatoro, Manuel; Guo, Jimin; Arakelian, Ani; Rabbani, Shafaat A.; Ali, Suhad; Lebrun, Jean Jacques

doi:10.1186/s13058-017-0831-8

Cited by 2 publications

(2 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in chondrocytes, TGF-β signaling stimulates cyclin D1 expression through activation of β-catenin signaling (Li et al 2006). Under certain circumstances, cyclin D1 can be manipulated as a downstream target of p21, a cell cycle negative regulator (Sandor et al 2000;Ungefroren et al 2011;Dai et al 2017). Nevertheless, the underlying molecular mechanism of how cyclin D1 expression is regulated by TGF-β signaling remains obscure and warrants future investigation.…”

Section: Discussionmentioning

confidence: 99%

Smad7 Regulates Dental Epithelial Proliferation during Tooth Development

et al. 2019

View full text Add to dashboard Cite

Tooth morphogenesis involves dynamic changes in shape and size as it proceeds through the bud, cap, and bell stages. This process requires exact regulation of cell proliferation and differentiation. Smad7, a general antagonist against transforming growth factor–β (TGF-β) signaling, is necessary for maintaining homeostasis and proper functionality in many organs. While TGF-β signaling is widely involved in tooth morphogenesis, the precise role of Smad7 in tooth development remains unknown. In this study, we showed that Smad7 is expressed in the developing mouse molars with a high level in the dental epithelium but a moderate to weak level in the dental mesenchyme. Smad7 deficiency led to a profound decrease in tooth size primarily due to a severely compromised cell proliferation capability in the dental epithelium. Consistent with the tooth shrinkage phenotype, RNA sequencing (RNA-seq) analysis revealed that Smad7 ablation downregulated genes referred to epithelial cell proliferation and cell cycle G1/S phase transition, whereas the upregulated genes were involved in responding to TGF-β signaling and cell cycle arrest. Among these genes, the expression of Cdkn1a (encoding p21), a negative cell proliferation regulator, was remarkably elevated in parallel with the diminution of Ccnd1 encoding the crucial cell cycle regulator cyclin D1 in the dental epithelium. Meanwhile, the expression level of p-Smad2/3 was ectopically elevated in the developing tooth germ of Smad7 null mice, indicating the hyperactivation of the canonical TGF-β signaling. These effects were reversed by addition of TGF-β signaling inhibitor in cell cultures of Smad7−/− molar tooth germs, with rescued expression of cyclin D1 and cell proliferation rate. In sum, our studies demonstrate that Smad7 functions primarily as a positive regulator of cell proliferation via inhibition of the canonical TGF-β signaling during dental epithelium development and highlight a crucial role for Smad7 in regulating tooth size.

show abstract

Section: Discussionmentioning

confidence: 99%

Smad7 Regulates Dental Epithelial Proliferation during Tooth Development

et al. 2019

View full text Add to dashboard Cite

show abstract

“…It also serves to enrich the population of cancer stem cells and induce angiogenesis. Cyclin D1 is a vital modulator of mammary and embryonic stem cells and is known to assist transforming growth factor β (TGF-β) in inducing stem cell renewal in triple-negative breast cancer cells [55,56]. Therefore, many promising studies have focussed on downregulating cyclin D1 for enhanced anticancer action [57][58][59][60].…”

Section: Activated Ampk Downregulates Cyclin Proteins and Induces Cel...mentioning

confidence: 99%

Targeting Breast Cancer and Their Stem Cell Population through AMPK Activation: Novel Insights

Uprety

Abrahamse

2022

Cells

View full text Add to dashboard Cite

Despite some significant advancements, breast cancer has become the most prevalent cancer in the world. One of the main reasons for failure in treatment and metastasis has been attributed to the presence of cancer initiating cells—cancer stem cells. Consequently, research is now being focussed on targeting cancer cells along with their stem cell population. Non-oncology drugs are gaining increasing attention for their potent anticancer activities. Metformin, a drug commonly used to treat type 2 diabetes, is the best example in this regard. It exerts its therapeutic action by activating 5′ adenosine monophosphate-activated protein kinase (AMPK). Activated AMPK subsequently phosphorylates and targets several cellular pathways involved in cell growth and proliferation and the maintenance of stem-like properties of cancer stem cells. Therefore, AMPK is emerging as a target of choice for developing effective anticancer drugs. Vanadium compounds are well-known PTP inhibitors and AMPK activators. They find extensive applications in treatment of diabetes and obesity via PTP1B inhibition and AMPK-mediated inhibition of adipogenesis. However, their role in targeting cancer stem cells has not been explored yet. This review is an attempt to establish the applications of insulin mimetic vanadium compounds for the treatment of breast cancer by AMPK activation and PTP1B inhibition pathways.

show abstract

Erratum to: Cyclin D1 cooperates with p21 to regulate TGFβ-mediated breast cancer cell migration and tumor local invasion

Cited by 2 publications

References 1 publication

Smad7 Regulates Dental Epithelial Proliferation during Tooth Development

Smad7 Regulates Dental Epithelial Proliferation during Tooth Development

Targeting Breast Cancer and Their Stem Cell Population through AMPK Activation: Novel Insights

Contact Info

Product

Resources

About