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719 results on '"Jiang WG"'

1. Role of the WASP and WAVE family proteins in breast cancer invasion and metastasis

Author

Frugtniet B, Jiang WG, and Martin TA

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Bethan Frugtniet, Wen G Jiang, Tracey A Martin Cardiff-China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff University, Cardiff, UKAbstract: The Wiskott–Aldrich syndrome protein (WASP) and WASP family verprolin-homologous protein (WAVE) family are a group of molecules that form a key link between GTPases and the actin cytoskeleton. The role of WASP/WAVE family proteins in the control of actin polymerization through activation of the actin-related protein 2/3 complex is critical in the formation of the actin-based membrane protrusions seen in cell migration and invasion. For this reason, the activity of the WASP/WAVE family in cancer cell invasion and migration has been of great interest in recent years. Many reports have highlighted the potential of targeting the WASP/WAVE family as a therapy for the prevention of cancer progression, in particular breast cancer. This review focuses on the role of the WASP/WAVE family in breast cancer cell invasion and migration and how this relates to the molecular mechanisms of WASP/WAVE activity, their exact contributions to the stages of cancer progression, and how this can lead to the development of anticancer drugs that target the WASP/WAVE family and related pathways.Keywords: WASP, WAVE, breast cancer, migration, invasion

Published
2015

2. The mRNA expression of SETD2 in human breast cancer: correlation with clinico-pathological parameters

Author

Al Sarakbi W, Sasi W, Jiang WG, Roberts T, Newbold RF, and Mokbel K

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background SET domain containing protein 2 (SETD2) is a histone methyltransferase that is involved in transcriptional elongation. There is evidence that SETD2 interacts with p53 and selectively regulates its downstream genes. Therefore, it could be implicated in the process of carcinogenesis. Furthermore, this gene is located on the short arm of chromosome 3p and we previously demonstrated that the 3p21.31 region of chromosome 3 was associated with permanent growth arrest of breast cancer cells. This region includes closely related genes namely: MYL3, CCDC12, KIF9, KLHL18 and SETD2. Based on the biological function of these genes, SETD2 is the most likely gene to play a tumour suppressor role and explain our previous findings. Our objective was to determine, using quantitative PCR, whether the mRNA expression levels of SETD2 were consistent with a tumour suppressive function in breast cancer. This is the first study in the literature to examine the direct relationship between SETD2 and breast cancer. Methods A total of 153 samples were analysed. The levels of transcription of SETD2 were determined using quantitative PCR and normalized against (CK19). Transcript levels within breast cancer specimens were compared to normal background tissues and analyzed against conventional pathological parameters and clinical outcome over a 10 year follow-up period. Results The levels of SETD2 mRNA were significantly lower in malignant samples (p = 0.0345) and decreased with increasing tumour stage. SETD2 expression levels were significantly lower in samples from patients who developed metastasis, local recurrence, or died of breast cancer when compared to those who were disease free for > 10 years (p = 0.041). Conclusion This study demonstrates a compelling trend for SETD2 transcription levels to be lower in cancerous tissues and in patients who developed progressive disease. These findings are consistent with a possible tumour suppressor function of this gene in breast cancer.

Published
2009
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3. The clinical and biological implications of the focal adhesion kinase pathway in ShenLingLan mediated suppression of cellular migration of ovarian cancer cells

Author

Owen S, Ruge F, Gao Y, Yang Y, Hou J, Chen J, Lane J, Wang H, Wei C, Yiling Wu, and Jiang WG

Subjects
0301 basic medicine, Pathology, medicine.medical_specialty, Cell, lcsh:Medicine, Metastasis, Focal adhesion, 03 medical and health sciences, 0302 clinical medicine, Medicine, Paxillin, biology, business.industry, lcsh:R, Cell migration, ShenLingLan, ovarian cancer, cell migration, FAK, paxillin, protein array, medicine.disease, R1, 030104 developmental biology, medicine.anatomical_structure, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Phosphorylation, Antibody, biological phenomena, cell phenomena, and immunity, business, Ovarian cancer
Abstract

The incidence of ovarian cancer in the UK has increased by almost twenty percent since the 1970’s and the majority of cases are not diagnosed until the late stages, when metastasis is more likely to have occurred. Focal Adhesion Kinase (FAK) is one of the key protein complexes which is integral to cell migration and has been linked to a variety of solid tumours. ShenLingLan (SLDM) is a traditional herbal medicine which has been formulated for the treatment of solid tumours. This study aimed to establish the impact of SLDM on FAK in ovarian cancer cells in vitro and transcript levels of FAK in an ovarian cancer cohort. FAK and paxillin phosphorylation events stimulated by SLDM treatment were identified using a Kinexus™ antibody based protein array. The impact of SLDM on cell attachment and migration was evaluated using Electric cell-substrate impedance sensing (ECIS), whilst the changes in focal adhesion complex localisation were assessed using immunofluorescence. In an ovarian cancer cohort, differences in FAK and paxillin transcript levels were assessed against key clinical parameters such as differentiation, stage and survival outcome. SLDM treatment of ovarian cancer cells in vitro resulted in the suppression of FAK and paxillin phosphorylation at several sites, which appeared to manifest as decreased cellular attachment and migration in a range of immortalised ovarian cancer cells. Increased FAK and paxillin transcript copies were observed in high grade and poorly differentiated ovarian tumours as well as in tumours from patients with ovarian cancer related incidence. SLDM has a profound effect on the migratory and adhesive properties of ovarian cancer cells, potentially via inhibitory effects on the activation of the FAK pathway, which is aberrant in clinical ovarian cancers.

Published
2017

13. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Block, KI, Gyllenhaal, C, Lowe, L, Amedei, A, Ruhul Amin, ARM, Amin, A, Aquilano, K, Arbiser, J, Arreola, A, Arzumanyan, A, Salman Ashraf, S, Azmi, AS, Benencia, F, Bhakta, D, Bilsland, A, Bishayee, A, Blain, SW, Block, PB, Boosani, CS, Carey, TE, Carnero, A, Carotenuto, M, Casey, SC, Chakrabarti, M, Chaturvedi, R, Chen, GZ, Chen, H, Chen, S, Chen, YC, Choi, BK, Ciriolo, MR, Coley, HM, Collins, AR, Connell, M, Crawford, S, Curran, CS, Dabrosin, C, Damia, G, Dasgupta, S, DeBerardinis, RJ, Decker, WK, Dhawan, P, Diehl, AME, Dong, JT, Dou, QP, Drewa, JE, Elkord, E, El-Rayes, B, Feitelson, MA, Felsheru, DW, Ferguson, LR, Fimognari, C, Firestone, GL, Frezza, C, Fujii, H, Fuster, MM, Generali, D, Georgakilas, AG, Gieseler, F, Gilbertson, M, Green, MF, Grue, B, Guhal, G, Halicka, D, Helferich, WG, Heneberg, P, Hentosh, P, Hirschey, MD, Hofseth, LJ, Holcombe, RF, Honoki, K, Hsu, HY, Huang, GS, Jensen, LD, Jiang, WG, Jones, LW, Karpowicz, PA, Keith, WN, Kerkar, SP, Khan, GN, Khatami, M, Ko, YH, Kucuk, O, Kulathinal, RJ, Kumar, NB, Kwon, BS, Leb, A, Leab, MA, Lee, HY, Lichtor, T, Lin, LT, and Locasale, JW

Abstract

© 2015 The Authors. Targeted therapies and the consequent adoption of "personalized" oncology have achieved notablesuccesses in some cancers; however, significant problems remain with this approach. Many targetedtherapies are highly toxic, costs are extremely high, and most patients experience relapse after a fewdisease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistantimmortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are notreliant upon the same mechanisms as those which have been targeted). To address these limitations, aninternational task force of 180 scientists was assembled to explore the concept of a low-toxicity "broad-spectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspectsof relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a widerange of high-priority targets (74 in total) that could be modified to improve patient outcomes. For thesetargets, corresponding low-toxicity therapeutic approaches were then suggested, many of which werephytochemicals. Proposed actions on each target and all of the approaches were further reviewed forknown effects on other hallmark areas and the tumor microenvironment. Potential contrary or procar-cinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixedevidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of therelationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. Thisnovel approach has potential to be relatively inexpensive, it should help us address stages and types ofcancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for futureresearch is offered.

Published
2015

20. Tuberin and hamartin are aberrantly expressed and linked to clinical outcome in human breast cancer: the role of promoter methylation of TSC genes

Author

Jiang, WG, Sampson, J, Martin, TA, Lee-Jones, L, Watkins, G, Douglas-Jones, A, Mokbel, K, Mansel, RE, Jiang, WG, Sampson, J, Martin, TA, Lee-Jones, L, Watkins, G, Douglas-Jones, A, Mokbel, K, and Mansel, RE

Abstract

Purpose: The tuberous sclerosis (TSC) genes TSC1 and TSC2 encode the protein products hamartin and tuberin, respectively, and are putative tumour suppressor genes. Germ-line mutation of either TSC gene leads to the development of the heritable disorder TSC. This disorder is characterized by the development of hamartomas in many organs and is associated with the proliferative lung disease, lymphangioleiomyomatosis, the brain tumour giant cell astrocytoma and occasionally with renal cell carcinoma. However, the TSC genes have not been studied in breast cancer. The current study investigated the expression of the TSC gene products and the potential mechanisms of their aberrancy in human breast cancer cells and tissues. Experimental design and results: Using immunohistochemical analysis, both hamartin and tuberin were found to be strongly stained in normal mammary epithelial cells and weakly in stromal cells. In invasive tumour tissues, however, the staining of both proteins were to be markedly reduced (P < 0.01). At message level, although normal and tumour tissues expressed both TSC products, the transcript levels of tuberin was significantly lower in tumour tissues compared with normal tissues (P < 0.05). There was no statistical difference between node negative and node positive tumours with both hamartin and tuberin. Tumours from patients who developed recurrence and died from breast cancer had significantly low levels of tuberin compared with those who remained disease free (P = 0.03 and 0.05, respectively). Likewise, hamartin levels were significantly lower in patients with metastasis, recurrence and mortality, when compared with those remained disease free (P = 0.001, 0.041 and 0.003, respectively). Using methylation specific PCR, the TSC1 promoter was found to be heavily methylated in ZR751, MDA MB 435, and BT549, but not in MCF-7 which expressed highly level of hamartin. TSC1 promoter methylation was also seen in most breast tumours, but only in a limited numb

Published
2005

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