Inhibition of cell proliferation, induction of apoptosis, reactivation of DLC1, and modulation of other gene expression by dietary flavone in breast cancer cell lines

Ullmannova, Veronika; Popescu, Nicholas C.

doi:10.1016/j.cdp.2007.02.005

Cited by 59 publications

(34 citation statements)

References 43 publications

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“…The potential treatment and prevention effects have been shown in degenerative diseases such as tumors, aging and cardiovascular diseases [10][11][12][13][14][15]. Additionally, some compounds of flavonoids possess potential application prospects as weak hormones at treating menopausal syndrome of women [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Isolation and Structure Identification of Flavonoids

Feng¹,

Hao²,

Li³

2017

Flavonoids - From Biosynthesis to Human Health

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Flavonoids, which possess a basic C15 phenyl-benzopyrone skeleton, refer to a series of compounds in which two benzene rings (ring A and B) are connected to each other through three carbon atoms. Based on their core structure, flavonoids can be grouped into different flavonoid classes, such as flavonols, flavones, flavanones, flavanonols, anthocyanidins, isoflavones and chalcones. Flavonoids are often hydroxylated in positions 3, 5, 7, 3 0 ,4 0 and/or 5 0 . Frequently, one or more of these hydroxyl groups are methylated, acetylated, prenylated or sulfated. In plants, flavonoids are often present as O-or C-glycosides. The O-glycosides have sugar substituents bound to a hydroxyl group of the aglycone, usually located at position 3 or 7, whereas the C-glycosides have sugar groups bound to a carbon of the aglycone, usually 6-C or 8-C. The most common carbohydrates are rhamnose, glucose, galactose and arabinose. This chapter mainly introduces the methods of isolation and structure identification of flavonoids.

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Section: Introductionmentioning

confidence: 99%

Isolation and Structure Identification of Flavonoids

Feng¹,

Hao²,

Li³

2017

Flavonoids - From Biosynthesis to Human Health

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“…The proliferation and apoptosis of tumour cells consist of a precise process regulated by multiple genes. Many studies both at home and abroad have demonstrated that flavonoid compounds can inhibit the proliferation of tumour cells, induce the apoptosis of tumour cells and regulate the expression of relevant genes to block the occurrence and development of tumour cells (12)(13)(14)(15). Isoquercitrin, the effective monomer from Bidens bipinnata L. extract, was used in the present study.…”

Section: Introductionmentioning

confidence: 99%

Isoquercitrin inhibits the progression of liver cancer in vivo and in vitro via the MAPK signalling pathway

Huang

Tang

et al. 2014

Oncology Reports

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Abstract. Liver cancer is a malignant tumour with high morbidity and fatality rates that is common worldwide. At present, the clinical approaches to treating primary liver cancer include partial hepatectomy, systemic or local chemotherapy, radiotherapy, radiofrequency ablative surgery and liver transplantation. However, all of these approaches have shortcomings, including poor prognosis and numerous side-effects. A large number of studies have proven that many effective ingredients in traditional Chinese medicine, particularly the flavonoid compounds extracted from plants, have achieved breakthroughs in terms of enhancing the effects and reducing the toxicity of chemotherapy and radiotherapy, preventing tumour metastasis and relapse after surgery, alleviating the clinical symptoms of advanced tumours, improving the quality of life of the patient with tumours and extending patient long-term survival. The purpose of the present study was to investigate the impact of isoquercitrin, the flavonoid from Bidens bipinnata L. extract, on the progression of liver cancer and to achieve a deeper understanding of the biological characteristics of isoquercitrin's involvement in the progression of liver cancer. In the in vitro experiments, isoquercitrin was found to strongly inhibit the proliferation of human liver cancer cells, promote the apoptosis of human liver cancer cells, and block the cell cycle in the G1 phase. Isoquercitrin activated caspase-3, -8 and -9, inhibited the expression level of ERK and p38MAPK protein phosphorylation, and promoted the phosphorylation of JNK. Additionally, isoquercitrin reduced the expression level of PKC in human liver cancer cells. In the in vivo experiments, isoquercitrin was also found to significantly inhibit the growth of transplanted tumours in nude mice. The present study confirmed that isoquercitrin could inhibit the progression of human liver cancer in vivo and in vitro, and the molecular mechanism of isoquercitrin may be closely associated with the MAPK and PKC signalling pathways.

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“…8,9 Loss of DLC1 expression, due to chromosomal deletion or promoter hypermethylation, has been detected in 50% of human hepatocellular carcinomas, and in many other human malignancies, including breast, prostate, colon, and lung. [10][11][12][13] Accordingly, therapeutic upregulation of DLC1 expression in cancer cells has been proposed as a novel method to induce apoptosis, and inhibit cell proliferation and colony formation, 14,15 and to restrain cell migration and suppress metastasis. [16][17][18] A key factor in the phosphatidylinositol-3-kinase (PI3K)/AKT signaling pathway is PIK3CA.…”

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confidence: 99%

Correlation of DLC1 gene methylation with oncogenic PIK3CA mutations in extramammary Paget's disease

Kang

Zhang

et al. 2012

Modern Pathology

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Extramammary Paget's disease is a rare cutaneous malignant neoplasm. The genetic and epigenetic mechanisms underlying its pathology remain unknown. In this study, we investigated the expression levels, and mutation and methylation status of a common tumor suppressor gene, deleted in liver cancer 1 (DLC1), and an oncogene, PIK3CA, in tumor (n ¼ 132) and normal tissues (n ¼ 20) from unrelated patients. The presence of epigenetic and genetic lesions was then correlated to the patient pathology data to determine the potential role of these genes in extramammary Paget's disease etiology and progression. The DLC1 gene was found to be downregulated in 43 (33%) tumors, as compared with immunohistochemistry results from normal tissues. Methylation-sensitive, high-resolution melting analysis indicated that the DLC1 promoter was hypermethylated in 51 (39%) extramammary Paget's disease tumors. This hypermethylation was associated with significantly decreased DLC1 levels (P ¼ 0.011), and had a strong positive correlation with advanced age (P ¼ 0.002). PIK3CA mutations were detected by direct sequencing in 32 (24%) tumors, the majority of which were invasive. Furthermore, PIK3CA mutations significantly correlated with DLC1 hypermethylation. Thus, aberrant DLC1 methylation and PIK3CA mutations may have important roles in extramammary Paget's disease pathogenesis, and may represent potential molecular targets for therapy.

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Inhibition of cell proliferation, induction of apoptosis, reactivation of DLC1, and modulation of other gene expression by dietary flavone in breast cancer cell lines

Cited by 59 publications

References 43 publications

Isolation and Structure Identification of Flavonoids

Isolation and Structure Identification of Flavonoids

Isoquercitrin inhibits the progression of liver cancer in vivo and in vitro via the MAPK signalling pathway

Correlation of DLC1 gene methylation with oncogenic PIK3CA mutations in extramammary Paget's disease

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