Colocalization of β-catenin with Notch intracellular domain in colon cancer: a possible role of Notch1 signaling in activation of CyclinD1-mediated cell proliferation

Gopalakrishnan, Natarajan; Marimuthu, Saravanakumar; Perumal, Madan Kumar; Thiyagu, Mani; Devaraj, Halagowder

doi:10.1007/s11010-014-2163-7

Cited by 46 publications

(45 citation statements)

References 48 publications

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“…Intriguingly, the favorable impact of high JAG1 expression on clinical outcome was particularly evident in tumors with negative nuclear b-catenin expression, which supports the well-described importance of the interconnection of the Wnt/b-catenin pathway (Balint et al 2005, Crosnier et al 2006, Wang et al 2009a, Yamamizu et al 2010, Kwon et al 2011, Peignon et al 2011, Kim et al 2012, Ravindran & Devaraj 2012, Gopalakrishnan et al 2014.…”

Section: Discussionsupporting

confidence: 67%

“…In particular, the link between Notch and Wnt/b-catenin signaling has been investigated in human development (Balint et al 2005, Crosnier et al 2006, Yamamizu et al 2010, Peignon et al 2011, Ravindran & Devaraj 2012, Gopalakrishnan et al 2014, and either additive or opposing effects have been reported, depending on the respective tissue and interfering factors (Kwon et al 2011, Kim et al 2012. Interestingly, Notch pathway activation has also been related, either alone or together, to Wnt/b-catenin activation and p53 deletion, to the epithelial-mesenchymal transition that is involved in the initiation of metastasis (Wang et al 2009a, Espinoza & Miele 2013, Chanrion et al 2014, and to resistance to treatment (Wang et al 2009b, Yao & Qian 2010, Ma et al 2013, Yoon et al 2014.…”

Section: Introductionmentioning

confidence: 99%

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Notch1 pathway in adrenocortical carcinomas: correlations with clinical outcome

Ronchi¹,

Sbiera²,

Altieri³

et al. 2015

Endocrine-Related Cancer

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Previous SNP array analyses have revealed genomic alterations of the Notch pathway as being the most frequent abnormality in adrenocortical tumors (ACTs). The aim of the present study was to evaluate the expression of components of Notch signaling in ACTs and to correlate them with clinical outcome. The mRNA expression of JAG1, NOTCH1, and selected target genes of NOTCH1 (HES1, HES5, and HEY2) was evaluated in 80 fresh frozen samples (28 normal adrenal glands (NAGs), 24 adenomas (ACAs), and 28 carcinomas (ACCs)) by quantitative RT-PCR. Immunohistochemistry was performed in 221 tissues on paraffin slides (16 NAGs, 27 ACAs, and 178 ACCs) for JAG1, activated NOTCH1 (aNOTCH1), and HEY2. An independent ACC validation cohort (nZ77) was then also investigated. HEY2 mRNA expression was higher in ACCs than it was in ACAs (P!0.05). The protein expression of all of the factors was high (H-score 2-3) in a larger proportion of ACCs as compared to ACAs and NAGs (JAG1 in 27, 15, and 10%; aNOTCH1 in 13, 8, and 0%; HEY2 in 66, 61, and 33% respectively, all P!0.001). High JAG1 expression was associated with earlier tumor stages and lower numbers of metastases in ACCs (both PZ0.08) and favorably impacted overall and progression-free survival (PFS) (131 vs 30 months, hazard ratio (HR) 0.45, and 37 vs 9 months, HR 0.51, both P!0.005). This impact on overall survival (OS) was confirmed in the validation cohort. No such association was observed for aNOTCH1 or HEY2. In conclusion, different components of the Notch1 signaling pathway are overexpressed in ACCs, which suggests a role for the pathway in malignant transformation. However, JAG1 is overexpressed in a subgroup of ACCs with a better clinical outcome.

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Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Notch1 pathway in adrenocortical carcinomas: correlations with clinical outcome

Ronchi¹,

Sbiera²,

Altieri³

et al. 2015

Endocrine-Related Cancer

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“…Therefore, any type of occurring disorder involving regulatory factors will lead to abnormal cell proliferation, thus inducing tumor formation and progression. Cyclin D1 can be combined with cyclin-dependent kinase 4 in the cell cycle to promote cell cycle progression, and therefore, is regarded as a type of proto-oncogene (28). Cyclin D1 protein expression is significantly correlated with colon cancer histology, presence of lymph node metastasis and staging, and colon cancer progression and metastasis (29).…”

Section: Discussionmentioning

confidence: 99%

Anticancer effect of icaritin inhibits cell growth of colon cancer through reactive oxygen species, Bcl-2 and cyclin D1/E signaling

Peng

Song

et al. 2016

Oncology Letters

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Abstract. Icaritin has an advantage in enhancing immunity. Besides, with its anticancer effect, it may be of great help in cancer treatment and recovery of cancer patients. As a result, icaritin is likely to become a novel anticancer drug. However, the anticancer effect of icaritin against colon cancer has not been elucidated thus far. The present study investigated the latent anticancer effect of icaritin on the inhibition of colon cancer cell growth by regulating reactive oxygen species (ROS), B-cell lymphoma (Bcl)-2 and cyclin D1/E signaling. The COLO-205 colon cancer cell line was used as a colon cancer cell model in the present study. First, cell growth and apoptosis were measured to analyze the anticancer effect of icaritin against colon cancer. Next, the possible mechanism of icaritin against colon cancer, including ROS, Bcl-2, cyclin D1, cyclin E and caspase-3/9, was explored. The results revealed that icaritin could inhibit cell growth and induce the apoptosis of COLO-205 cells. In addition, icaritin significantly induced ROS generation, suppressed Bcl-2, cyclin D1 and cyclin E protein expression, and activated caspase-3/9 activity in COLO-205 cells. The present findings demonstrated that icaritin exerted antiproliferative and anticancer effects against colon cancer through the activation of ROS generation and the suppression of Bcl-2, cyclin D1 and cyclin E signaling.

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“…We also identified increased expression of the connective tissue growth factor gene (Ctgf), which encodes a trophic factor known to stimulate NotchR and Wnt signaling (41), and the parkin2 gene (Park2), which is involved in mitophagy (42). The most downregulated genes included several cell cycle genes, encoding cyclin D1 (Ccnd1), cyclin A2 (Ccna2), and cyclin-dependent phosphatase (Cdc14a), all of which are known to be regulated by NotchRs or NotchR signals (43)(44)(45); a gene encoding a suppressor of cytokine signaling 2, a regulator of Jak-Stat signaling (46); one Wnt receptor gene (Fzd6) (47); and an insulin-like growth factor binding protein gene (Igfa1) (48). Several other genes tested were not significantly changed.…”

Section: Resultsmentioning

confidence: 99%

Deletion of Pofut1 in Mouse Skeletal Myofibers Induces Muscle Aging-Related Phenotypes in cis and in trans

Zygmunt

Singhal

Kim

et al. 2017

Molecular and Cellular Biology

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Sarcopenia, the loss of muscle mass and strength during normal aging, involves coordinate changes in skeletal myofibers and the cells that contact them, including satellite cells and motor neurons. Here we show that the protein Ofucosyltransferase 1 gene (Pofut1), which encodes a glycosyltransferase required for NotchR-mediated cell-cell signaling, has reduced expression in aging skeletal muscle. Moreover, premature postnatal deletion of Pofut1 in skeletal myofibers can induce aging-related phenotypes in cis within skeletal myofibers and in trans within satellite cells and within motor neurons via the neuromuscular junction. Changed phenotypes include reduced skeletal muscle size and strength, decreased myofiber size, increased slow fiber (type 1) density, increased muscle degeneration and regeneration in aged muscles, decreased satellite cell self-renewal and regenerative potential, and increased neuromuscular fragmentation and occasional denervation. Pofut1 deletion in skeletal myofibers reduced NotchR signaling in young adult muscles, but this effect was lost with age. Increasing muscle NotchR signaling also reduced muscle size. Gene expression studies point to regulation of cell cycle genes, muscle myosins, NotchR and Wnt pathway genes, and connective tissue growth factor by Pofut1 in skeletal muscle, with additional effects on ␣ dystroglycan glycosylation.KEYWORDS Notch signaling, glycobiology, muscle aging, sarcopenia S arcopenia, the loss of muscle mass and strength during the course of normal aging, has a profound impact on quality of life for the elderly (1-4). About one third of the muscle mass present in young individuals is lost during the aging process. Increased muscle weakness with age can result in decreased ambulation and in more frequent falls and bone fractures. Sarcopenia encompasses a number of phenotypic changes in skeletal muscle, including muscle atrophy, functional reductions in overall muscle strength, muscle wasting, neuromuscular decay and denervation, alterations in muscle fiber populations and patterning, reduced mitochondrial capacity, and the decreased regenerative capacity of satellite cells. Myriad changes in signaling cascades, endocrine hormones, inflammatory factors, ␤ agonists, muscle factors, antioxidants, and energy metabolites have been suggested as contributing factors to sarcopenia, many of them by altering downstream myogenic regulatory factors (1, 2, 4). Similarly, there are a number of factors that control aging in a more global manner (IgfRs, Klotho, p53, Ku-80,

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Colocalization of β-catenin with Notch intracellular domain in colon cancer: a possible role of Notch1 signaling in activation of CyclinD1-mediated cell proliferation

Cited by 46 publications

References 48 publications

Notch1 pathway in adrenocortical carcinomas: correlations with clinical outcome

Notch1 pathway in adrenocortical carcinomas: correlations with clinical outcome

Anticancer effect of icaritin inhibits cell growth of colon cancer through reactive oxygen species, Bcl-2 and cyclin D1/E signaling

Deletion of Pofut1 in Mouse Skeletal Myofibers Induces Muscle Aging-Related Phenotypes in cis and in trans

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