Abstract A40: Protein disulfide isomerases in the endoplasmic reticulum promote anchorage-independent growth of breast cancer cells

2016 ◽  
Author(s):  
Randi Wise ◽  
Sara Duhachek-Muggy ◽  
Yue Qi ◽  
Michal Zolkiewski ◽  
Anna Zolkiewska
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Anchorage Independent Growth ◽  
Protein Disulfide Isomerases ◽  
Disulfide Isomerases ◽  
Protein Disulfide

scholarly journals CBIO-29. ACOT7 REGULATES COLONIZATION OF BREAST CANCER CELLS IN THE BRAIN BY REGULATING ENDOPLASMIC RETICULUM STRESS RESPONSE

2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi38-vi38
Author(s):  
Deepak Kanojia ◽  
Wojciech K Panek ◽  
Alex Cordero ◽  
Annie Xiao ◽  
Jason Miska ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Endoplasmic Reticulum Stress Response ◽  
The Brain

RSK2 protects human breast cancer cells under endoplasmic reticulum stress through activating AMPKα2-mediated autophagy

Oncogene ◽  
2020 ◽  
Vol 39 (43) ◽  
pp. 6704-6718
Author(s):  
Lan-Ya Li ◽  
Xi-Sha Chen ◽  
Kuan-Song Wang ◽  
Yi-Di Guan ◽  
Xing-Cong Ren ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Synthesis and Pharmacological Characterization of 2-Aminoethyl Diphenylborinate (2-APB) Derivatives for Inhibition of Store-Operated Calcium Entry (SOCE) in MDA-MB-231 Breast Cancer Cells

2020 ◽  
Vol 21 (16) ◽  
pp. 5604 ◽  
Author(s):  
Achille Schild ◽  
Rajesh Bhardwaj ◽  
Nicolas Wenger ◽  
Dominic Tscherrig ◽  
Palanivel Kandasamy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Structural Changes ◽  
Calcium Entry ◽  
Imaging Plate ◽  
Ip3 Receptors ◽  
Pharmacological Characterization ◽  
Store Operated Calcium Entry

Calcium ions regulate a wide array of physiological functions including cell differentiation, proliferation, muscle contraction, neurotransmission, and fertilization. The endoplasmic reticulum (ER) is the major intracellular Ca2+ store and cellular events that induce ER store depletion (e.g., activation of inositol 1,4,5-triphosphate (IP3) receptors) trigger a refilling process known as store-operated calcium entry (SOCE). It requires the intricate interaction between the Ca2+ sensing stromal interaction molecules (STIM) located in the ER membrane and the channel forming Orai proteins in the plasma membrane (PM). The resulting active STIM/Orai complexes form highly selective Ca2+ channels that facilitate a measurable Ca2+ influx into the cytosol followed by successive refilling of the ER by the sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA). STIM and Orai have attracted significant therapeutic interest, as enhanced SOCE has been associated with several cancers, and mutations in STIM and Orai have been linked to immunodeficiency, autoimmune, and muscular diseases. 2-Aminoethyl diphenylborinate (2-APB) is a known modulator and depending on its concentration can inhibit or enhance SOCE. We have synthesized several novel derivatives of 2-APB, introducing halogen and other small substituents systematically on each position of one of the phenyl rings. Using a fluorometric imaging plate reader (FLIPR) Tetra-based calcium imaging assay we have studied how these structural changes of 2-APB affect the SOCE modulation activity at different compound concentrations in MDA-MB-231 breast cancer cells. We have discovered 2-APB derivatives that block SOCE at low concentrations, at which 2-APB usually enhances SOCE.

scholarly journals Loss of STAT6 leads to anchorage-independent growth and trastuzumab resistance in HER2+ breast cancer cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (6) ◽  
pp. e0234146 ◽  
Author(s):  
Molly DiScala ◽  
Matthew S. Najor ◽  
Timothy Yung ◽  
Deri Morgan ◽  
Abde M. Abukhdeir ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Trastuzumab Resistance ◽  
Anchorage Independent Growth ◽  
Her2 Breast Cancer

scholarly journals High concentration calcitriol induces endoplasmic reticulum stress related gene profile in breast cancer cells

2017 ◽  
Vol 95 (2) ◽  
pp. 289-294 ◽  
Author(s):  
Ali Burak Ozkaya ◽  
Handan Ak ◽  
Hikmet Hakan Aydin
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Survival Function ◽  
Active Form ◽  
Breast Cancer Cell Lines ◽  
Transcriptomic Profile

Calcitriol, the active form of vitamin D, is known for its anticancer properties including induction of apoptosis as well as the inhibition of angiogenesis and metastasis. Understanding the mechanisms of action for calcitriol will help with the development of novel treatment strategies. Since vitamin D exerts its cellular actions via binding to its receptor and by altering expressions of a set of genes, we aimed to evaluate the effect of calcitriol on transcriptomic profile of breast cancer cells. We previously demonstrated that calcitriol alters endoplasmic reticulum (ER) stress markers, therefore in this study we have focused on ER-stress-related genes to reveal calcitriols action on these genes in particular. We have treated breast cancer cell lines MCF-7 and MDA-MB-231 with previously determined IC50 concentrations of calcitriol and evaluated the transcriptomic alterations via microarray. During analysis, only genes altered by at least 2-fold with a P value < 0.05 were taken into consideration. Our findings revealed an ER-stress-associated transcriptomic profile induced by calcitriol. Induced genes include genes with a pro-survival function (NUPR1, DNAJB9, HMOX1, LCN2, and LAMP3) and with a pro-death function (CHOP (DDIT3), DDIT4, NDGR1, NOXA, and CLGN). These results suggest that calcitriol induces an ER-stress-like response inducing both pro-survival and pro-death transcripts in the process.

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