scholarly journals Adenomatous Polyposis Coli and Ras Association Domain Family 1A Gene Methylation in Breast Cancer Patients

2007 ◽  
Vol 10 (2) ◽  
pp. 120
Author(s):  
Il-kyung Park ◽  
Jee-Soo Yim ◽  
Yu-Mi Ra ◽  
Dae-gyung Ko ◽  
In-seok Choi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Adenomatous Polyposis Coli ◽  
Adenomatous Polyposis ◽  
Breast Cancer Patients ◽  
Polyposis Coli ◽  
Domain Family ◽  
Gene Methylation

scholarly journals Adenomatous Polyposis Coli Loss Controls Cell Cycle Regulators and Response to Paclitaxel

2020 ◽  
Author(s):  
Emily M. Astarita ◽  
Camden A. Hoover ◽  
Sara M. Maloney ◽  
T. Murlidharan Nair ◽  
Jenifer R. Prosperi
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Adenomatous Polyposis Coli ◽  
Cyclin B1 ◽  
Cell Cycle Analysis ◽  
Specific Cell ◽  
Breast Cancers ◽  
Cell Cycle Regulators ◽  
Adenomatous Polyposis ◽  
Polyposis Coli

AbstractAdenomatous Polyposis Coli (APC) is lost in approximately 70% of sporadic breast cancers, with an inclination towards triple negative breast cancer (TNBC). TNBC is treated with traditional chemotherapy, such as paclitaxel (PTX); however, tumors often develop drug resistance. We previously created APC knockdown cells (APC shRNA1) using the human TNBC cells, MDA-MB-157, and showed that APC loss induces PTX resistance. To understand the mechanisms behind APC-mediated PTX response, we performed cell cycle analysis and analyzed cell cycle related proteins. Cell cycle analysis indicated increased G2/M population in PTX-treated APC shRNA1 cells compared to PTX-treated controls, suggesting that APC expression does not alter PTX-induced G2/M arrest. We further studied the subcellular localization of the G2/M transition proteins, cyclin B1 and CDK1. The APC shRNA1 cells had increased CDK1, which was preferentially localized to the cytoplasm, and increased CDK6. RNA-sequencing was performed to gain a global understanding of changes downstream of APC loss and identified a broad mis-regulation of cell cycle-related genes in APC shRNA1 cells. Our studies are the first to show an interaction between APC and taxane response in breast cancer. The implications include designing combination therapy to re-sensitize APC-mutant breast cancers to taxanes using the specific cell cycle alterations.

β-Catenin and adenomatous polyposis coli (APC) mutations in adenomas from hereditary non-polyposis colorectal cancer patients

2000 ◽  
Vol 157 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Yoshimitsu Akiyama ◽  
Hiromi Nagasaki ◽  
Kenji Osmar Yagi ◽  
Tadashi Nomizu ◽  
Yasuhito Yuasa
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Adenomatous Polyposis Coli ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Apc Mutations ◽  
Colorectal Cancer Patients

MUC1 can interact with adenomatous polyposis coli in breast cancer

2004 ◽  
Vol 316 (2) ◽  
pp. 364-369 ◽  
Author(s):  
Christine L Hattrup ◽  
Julia Fernandez-Rodriguez ◽  
Joyce A Schroeder ◽  
Gunnar C Hansson ◽  
Sandra J Gendler
Keyword(s):  
Breast Cancer ◽  
Adenomatous Polyposis Coli ◽  
Adenomatous Polyposis ◽  
Polyposis Coli

scholarly journals Analysing the mutational status of adenomatous polyposis coli (APC) gene in breast cancer

2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Ya-Sian Chang ◽  
Chien-Yu Lin ◽  
Shu-Fen Yang ◽  
Cheng-Mao Ho ◽  
Jan-Gowth Chang
Keyword(s):  
Breast Cancer ◽  
Adenomatous Polyposis Coli ◽  
Apc Gene ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Mutational Status
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