scholarly journals Aurora kinase A stabilizes FOXM1 to enhance paclitaxel resistance in triple‐negative breast cancer

2019 ◽  
Vol 23 (9) ◽  
pp. 6442-6453 ◽  
Author(s):  
Na Yang ◽  
Chang Wang ◽  
Jian Wang ◽  
Zifeng Wang ◽  
Di Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Aurora Kinase ◽  
Paclitaxel Resistance ◽  
Aurora Kinase A ◽  
Kinase A

scholarly journals p53 Family Members Regulate Phenotypic Response to Aurora Kinase A Inhibition in Triple-Negative Breast Cancer

2015 ◽  
Vol 14 (5) ◽  
pp. 1117-1129 ◽  
Author(s):  
John J. Tentler ◽  
Anastasia A. Ionkina ◽  
Aik Choon Tan ◽  
Timothy P. Newton ◽  
Todd M. Pitts ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Family Members ◽  
Aurora Kinase ◽  
P53 Family ◽  
Aurora Kinase A ◽  
Phenotypic Response ◽  
Kinase A

scholarly journals Targeting the Id1-Kif11 Axis in Triple-Negative Breast Cancer Using Combination Therapy

Biomolecules ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1295
Author(s):  
Archana P. Thankamony ◽  
Reshma Murali ◽  
Nitheesh Karthikeyan ◽  
Binitha Anu Varghese ◽  
Wee S. Teo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Triple Negative Breast Cancer ◽  
Large Scale ◽  
Triple Negative ◽  
Genomic Analysis ◽  
Aurora Kinase ◽  
Cell Cycle Regulators ◽  
Tumor Models ◽  
Tnbc Subtype

The basic helix-loop-helix (bHLH) transcription factors inhibitor of differentiation 1 (Id1) and inhibitor of differentiation 3 (Id3) (referred to as Id) have an important role in maintaining the cancer stem cell (CSC) phenotype in the triple-negative breast cancer (TNBC) subtype. In this study, we aimed to understand the molecular mechanism underlying Id control of CSC phenotype and exploit it for therapeutic purposes. We used two different TNBC tumor models marked by either Id depletion or Id1 expression in order to identify Id targets using a combinatorial analysis of RNA sequencing and microarray data. Phenotypically, Id protein depletion leads to cell cycle arrest in the G0/G1 phase, which we demonstrate is reversible. In order to understand the molecular underpinning of Id proteins on the cell cycle phenotype, we carried out a large-scale small interfering RNA (siRNA) screen of 61 putative targets identified by using genomic analysis of two Id TNBC tumor models. Kinesin Family Member 11 (Kif11) and Aurora Kinase A (Aurka), which are critical cell cycle regulators, were further validated as Id targets. Interestingly, unlike in Id depletion conditions, Kif11 and Aurka knockdown leads to a G2/M arrest, suggesting a novel Id cell cycle mechanism, which we will explore in further studies. Therapeutic targeting of Kif11 to block the Id1–Kif11 axis was carried out using small molecular inhibitor ispinesib. We finally leveraged our findings to target the Id/Kif11 pathway using the small molecule inhibitor ispinesib in the Id+ CSC results combined with chemotherapy for better response in TNBC subtypes. This work opens up exciting new possibilities of targeting Id targets such as Kif11 in the TNBC subtype, which is currently refractory to chemotherapy. Targeting the Id1–Kif11 molecular pathway in the Id1+ CSCs in combination with chemotherapy and small molecular inhibitor results in more effective debulking of TNBC.

Polymer Nanovesicle-Mediated Delivery of MLN8237 Preferentially Inhibits Aurora Kinase A To Target RalA and Anchorage-Independent Growth in Breast Cancer Cells

2018 ◽  
Vol 15 (8) ◽  
pp. 3046-3059
Author(s):  
Siddhi Inchanalkar ◽  
Nilesh Umakant Deshpande ◽  
Vishakha Kasherwal ◽  
Manickam Jayakannan ◽  
Nagaraj Balasubramanian
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Aurora Kinase ◽  
Aurora Kinase A ◽  
Anchorage Independent Growth ◽  
Kinase A
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