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Low-dose irradiation promotes proliferation of the human breast cancer MDA-MB-231 cells through accumulation of mutant P53.
Abstract Low-dose irradiation (LDIR) has been proven to have differential biological effects on normal mammalian somatic cells and cancer cells. Our previous study showed that p53 gene status is a critical factor regulating the effect of LDIR on cancer cells. We investigated the effect of LDIR on the breast cancer cell line MDA-MB-231 that harbors a mutant p53 gene, and the normal breast fibroblast cell line Hs 578Bst. In the present study, we showed that 150 mGy LDIR pormoted growth of MDA-MB-231 cells but not Hs 578Bst cells. Through cell cycle analyses, we found that LDIR accelerated cell cycle into S phase i...
Source: International Journal of Oncology - December 5, 2016 Category: Cancer & Oncology Authors: Li SJ, Liang XY, Li HJ, Li W, Zhou L, Chen HQ, Ye SG, Yu DH, Cui JW Tags: Int J Oncol Source Type: research

IGF-1R inhibition sensitizes breast cancer cells to ATM-Related Kinase (ATR) inhibitor and cisplatin.
Authors: O'Flanagan CH, O'Shea S, Lyons A, Fogarty FM, McCabe N, Kennedy RD, O'Connor R Abstract The complexity of the IGF-1 signalling axis is clearly a roadblock in targeting this receptor in cancer therapy. Here, we sought to identify mediators of resistance, and potential co-targets for IGF-1R inhibition. By using an siRNA functional screen with the IGF-1R tyrosine kinase inhibitor (TKI) BMS-754807 in MCF-7 cells we identified several genes encoding components of the DNA damage response (DDR) pathways as mediators of resistance to IGF-1R kinase inhibition. These included ATM and Ataxia Telangiectasia and RAD3-r...
Source: Oncotarget - July 30, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Abstract 5193: Ataxia telangiectasia mutated relates to epithelial-mesenchymal transition in colorectal cancer
Conclusions: ATM might be a critical regulator of EMT in colorectal cancer invasion.Citation Format: Hidena Takahashi, Masashi Tsuruta, Hirotoshi Hasegawa, Koji Okabayashi, Ryo Seishima, Shimpei Matsui, Toru Yamada, Takayuki Kondo, Takehiro Shimada, Mutsuhito Matsuda, Masashi Yahagi, Yusuke Yoshikawa, Yusuke Asada, Kiyoaki Sugiura, Yoshiyuki Suzuki, Yuki Tajima, Junpei Nakadai, Yuko Kitagawa. Ataxia telangiectasia mutated relates to epithelial-mesenchymal transition in colorectal cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Takahashi, H., Tsuruta, M., Hasegawa, H., Okabayashi, K., Seishima, R., Matsui, S., Yamada, T., Kondo, T., Shimada, T., Matsuda, M., Yahagi, M., Yoshikawa, Y., Asada, Y., Sugiura, K., Suzuki, Y., Tajima, Y., Nakadai, J., Kitagawa, Y. Tags: Tumor Biology Source Type: research

Polycation-functionalized nanoporous silicon particles for gene silencing on breast cancer cells.
Abstract Nanoporous silicon particles (pSi), with a pore size in the range of 20-60 nm, were modified with polyethyleneimine (PEI) to yield pSi-PEI particles, which were subsequently complexed with siRNA. Thus, pSi-PEI/siRNA particles were fabricated, with the PEI/siRNA nanocomplexes mainly anchored inside the nanopore of the pSi particles. These hybrid particles were used as carriers to deliver siRNA to human breast cancer cells. Due to the gradual degradation of the pSi matrix under physiological conditions, the PEI/siRNA nanocomplexes were released from the pore interior in a sustained manner. Physicochemical ...
Source: Biomaterials - October 5, 2013 Category: Materials Science Authors: Zhang M, Xu R, Xia X, Yang Y, Gu J, Qin G, Liu X, Ferrari M, Shen H Tags: Biomaterials Source Type: research

Nuclear Import of HBXIP Requires Collaboration with c-Fos Gene Regulation
Aberrant nuclear localization of oncogenic transcription factors and coactivators always leads to the development of cancer. We have reported that the oncoprotein hepatitis B X-interacting protein (HBXIP) acts as a novel transcriptional coactivator to promote proliferation and migration of breast cancer cells. However, the mechanism of regulating the nuclear import of HBXIP remains unclear. In the present study, we found that HBXIP interacted with c-Fos through their leucine zipper domains in vitro and in vivo. Interestingly, the leucine zipper mutant of HBXIP (or c-Fos) was unavailable to bind to c-Fos (or HBXIP), resulti...
Source: Journal of Biological Chemistry - June 28, 2013 Category: Chemistry Authors: Zhang, Y., Zhao, Y., Li, H., Li, Y., Cai, X., Shen, Y., Shi, H., Li, L., Liu, Q., Zhang, X., Ye, L. Tags: Cell Biology Source Type: research