scholarly journals Substantial cell apoptosis provoked by Naked PAMAM Dendrimers in HER2-positive human breast cancer via JNK and ERK1/ERK2 signalling pathways

Author(s):  
Hadeel Kheraldine ◽  
Ishita Gupta ◽  
Hashim Alhussain ◽  
Aayesha Jabeen ◽  
Farhan S. Cyprian ◽  
...  
2013 ◽  
Vol 65 (3) ◽  
pp. 341-349 ◽  
Author(s):  
Sujatha Ramasamy ◽  
Norhanom Abdul Wahab ◽  
Nurhayati Zainal Abidin ◽  
Sugumaran Manickam

2014 ◽  
Vol 21 (5) ◽  
pp. X1-X3 ◽  
Author(s):  
M. McIlroy ◽  
F. J. Fleming ◽  
Y. Buggy ◽  
A. D. K. Hill ◽  
L. S. Young

2006 ◽  
Vol 13 (4) ◽  
pp. 1135-1145 ◽  
Author(s):  
Marie Mc Ilroy ◽  
Fergal J Fleming ◽  
Yvonne Buggy ◽  
Arnold D K Hill ◽  
Leonie S Young

Differential signalling between the two oestrogen receptor (ER) isoforms in the presence of tamoxifen has been described. We hypothesise that differential recruitment of the steroid receptor co-activator, SRC-3 to ER-α and ER-β may in part explain associations between ER isoforms and response to endocrine treatment. SRC-3 was localised within epithelial cells of breast tumour tissue and was co-localised with ER-α and ER-β, (n = 112). Expression of SRC-3 was found to be positively associated with ER-α (P = 0.0021) and inversely with ER-β (P < 0.0001). Uniquely, this study utilises primary cell cultures derived from patient tumours, thus providing samples not readily available in most molecular model systems. These samples have enabled us to investigate the influence of growth factor pathways on steroid receptor-co-activator interactions. In HER2 (human epidermal growth factor receptor 2) positive primary tumour cell cultures 17β-estradiol induced a decrease in SRC-3, whereas upregulated SRC-3 expression. Furthermore, treatment with tamoxifen-induced SRC-3 recruitment to the ER-oestrogen response element and enhanced interaction between SRC-3 and ER-α, but not ER-β. Knockdown of SRC-3 results in a concomitant loss of expression of the oestrogen target gene pS2. Furthermore, silencing of SRC-3 resensitizes endocrine resistant, HER2 positive cells to the anti-proliferative effects of tamoxifen. The ability of ER-α, but not ER-β to recruit SRC-3 in the presence of tamoxifen may in part explain the differential ER isoform associations with recurrence in human breast cancer.


2017 ◽  
Vol 14 (4) ◽  
pp. 3947-3952 ◽  
Author(s):  
Yu Lu ◽  
Yanyan Li ◽  
Min Xiang ◽  
Jie Zhou ◽  
Juan Chen

Open Biology ◽  
2016 ◽  
Vol 6 (12) ◽  
pp. 150262 ◽  
Author(s):  
Chin-Yo Lin ◽  
Erica L. Kleinbrink ◽  
Fabien Dachet ◽  
Juan Cai ◽  
Donghong Ju ◽  
...  

Long non-coding RNAs (lncRNAs) are transcripts of a recently discovered class of genes which do not code for proteins. LncRNA genes are approximately as numerous as protein-coding genes in the human genome. However, comparatively little remains known about lncRNA functions. We globally interrogated changes in the lncRNA transcriptome of oestrogen receptor positive human breast cancer cells following treatment with oestrogen, and identified 127 oestrogen-responsive lncRNAs. Consistent with the emerging evidence that most human lncRNA genes lack homologues outside of primates, our evolutionary analysis revealed primate-specific lncRNAs downstream of oestrogen signalling. We demonstrate, using multiple functional assays to probe gain- and loss-of-function phenotypes in two oestrogen receptor positive human breast cancer cell lines, that two primate-specific oestrogen-responsive lncRNAs identified in this study (the oestrogen-repressed lncRNA BC041455, which reduces cell viability, and the oestrogen-induced lncRNA CR593775, which increases cell viability) exert previously unrecognized functions in cell proliferation and growth factor signalling pathways. The results suggest that oestrogen-responsive lncRNAs are capable of altering the proliferation and viability of human breast cancer cells. No effects on cellular phenotypes were associated with control transfections. As heretofore unappreciated components of key signalling pathways in cancers, including the MAP kinase pathway, lncRNAs hence represent a novel mechanism of action for oestrogen effects on cellular proliferation and viability phenotypes. This finding warrants further investigation in basic and translational studies of breast and potentially other types of cancers, has broad relevance to lncRNAs in other nuclear hormone receptor pathways, and should facilitate exploiting and targeting these cell viability modulating lncRNAs in post-genomic therapeutics.


2018 ◽  
Vol 6 (5) ◽  
pp. 1217-1226 ◽  
Author(s):  
Kyoung Sub Kim ◽  
Jiyoung Kim ◽  
Da Hye Kim ◽  
Hee Sook Hwang ◽  
Kun Na

Effective penetration and targeted delivery of anticancer drugs into tumor tissues are limiting factors for achieving enhanced therapeutic efficacy.


2015 ◽  
Vol 15 (24) ◽  
pp. 10659-10663 ◽  
Author(s):  
Tengku Ahmad Damitri Al-Astani Tengku Din ◽  
Azman Seeni ◽  
Wirdatul-Nur Mohd Khairi ◽  
Shaharum Shamsuddin ◽  
Hasnan Jaafar

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