scholarly journals Dysregulated connexin 43 in HER2-positive drug resistant breast cancer cells enhances proliferation and migration

Oncotarget ◽  
2017 ◽  
Vol 8 (65) ◽  
pp. 109358-109369 ◽  
Author(s):  
Elizabeth S. Yeh ◽  
Christina J. Williams ◽  
Carly Bess Williams ◽  
Ingrid V. Bonilla ◽  
Nancy Klauber-DeMore ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Connexin 43 ◽  
Breast Cancer Cells ◽  
Drug Resistant ◽  
Her2 Positive ◽  
And Migration ◽  
Proliferation And Migration

Amphiregulin regulates proliferation and migration of HER2-positive breast cancer cells

2017 ◽  
Vol 41 (2) ◽  
pp. 159-168 ◽  
Author(s):  
Hannah Schmucker ◽  
Walker M. Blanding ◽  
Julia M. Mook ◽  
Jessica F. Wade ◽  
Jang Pyo Park ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Her2 Positive ◽  
Her2 Positive Breast Cancer ◽  
And Migration ◽  
Proliferation And Migration ◽  
Positive Breast Cancer

scholarly journals miR-145 inhibits proliferation and migration of breast cancer cells by directly or indirectly regulating TGF-β1 expression

2017 ◽  
Vol 50 (5) ◽  
pp. 1701-1710 ◽  
Author(s):  
Yanling Ding ◽  
Chunfu Zhang ◽  
Jiahui Zhang ◽  
Nannan Zhang ◽  
Tao Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

scholarly journals MARK4 inhibits Hippo signaling to promote proliferation and migration of breast cancer cells

EMBO Reports ◽  
2017 ◽  
Vol 18 (3) ◽  
pp. 420-436 ◽  
Author(s):  
Emad Heidary Arash ◽  
Ahmed Shiban ◽  
Siyuan Song ◽  
Liliana Attisano
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Hippo Signaling ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Aberrant ALOX5 Activation Correlates with HER2 Status and Mediates Breast Cancer Biological Activities through Multiple Mechanisms

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Xiao Zhou ◽  
Yi Jiang ◽  
Qiuyun Li ◽  
Zhen Huang ◽  
Huawei Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biological Activities ◽  
Critical Role ◽  
Her2 Overexpression ◽  
Her2 Positive ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Expression And Activity

Arachidonate lipoxygenases (ALOX) have been implicated in playing a critical role in tumorigenesis, development, and metastasis. We previously reported that ALOX12 is involved in breast cancer chemoresistance. In this study, we demonstrate that the ALOX5 activation correlates with the HER2 expression and mediates breast cancer growth and migration. We found that the ALOX5 expression and activity were upregulated in breast cancer patients, particularly in those tissues with HER2-positive. ALOX5 upregulation was also observed in HER2-positive breast cancer cells. In contrast, HER2 inhibition led to decreased expression and activity of ALOX5 but not ALOX5AP, suggesting that HER2 specifically regulates the ALOX5 expression and activity in breast cancer cells. We further demonstrated that ALOX5 is important for breast cancer biological activities with the predominant roles in growth and migration, likely through RhoA, focal adhesion, and PI3K/Akt/mTOR signaling but not epithelial mesenchymal transition (EMT). Our work is the first to report a correlation between the ALOX5 activity and HER2 overexpression in breast cancer. Our findings also highlight the therapeutic value of inhibiting ALOX5 in breast cancer, particularly those patients with the HER2 overexpression.

scholarly journals PGC-1β cooperating with FOXA2 inhibits proliferation and migration of breast cancer cells

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jia Cao ◽  
Xi Wang ◽  
Danni Wang ◽  
Rong Ma ◽  
Xiaohan Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Modulation of the uptake of critical nutrients by breast cancer cells by lactate: Impact on cell survival, proliferation and migration

2016 ◽  
Vol 341 (2) ◽  
pp. 111-122 ◽  
Author(s):  
Marta Guedes ◽  
João R. Araújo ◽  
Ana Correia-Branco ◽  
Inês Gregório ◽  
Fátima Martel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
And Migration ◽  
Critical Nutrients ◽  
Proliferation And Migration

scholarly journals Transient Receptor Potential Melastatin 8 (TRPM8) Channel Regulates Proliferation and Migration of Breast Cancer Cells by Activating the AMPK-ULK1 Pathway to Enhance Basal Autophagy

2020 ◽  
Vol 10 ◽  
Author(s):  
Yuan Huang ◽  
Shi Li ◽  
Zhenhua Jia ◽  
Weiwei Zhao ◽  
Cefan Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Melastatin ◽  
Ampk Activity ◽  
Transient Receptor ◽  
And Migration ◽  
Proliferation And Migration

The calcium-permeable cation channel TRPM8 (transient receptor potential melastatin 8) is a member of the TRP superfamily of cation channels that is upregulated in various types of cancer with high levels of autophagy, including prostate, pancreatic, breast, lung, and colon cancers. Autophagy is closely regulated by AMP-activated protein kinase (AMPK) and plays an important role in tumor growth by generating nutrients through degradation of intracellular structures. Additionally, AMPK activity is regulated by intracellular Ca2+ concentration. Considering that TRPM8 is a non-selective Ca2+-permeable cation channel and plays a key role in calcium homoeostasis, we hypothesized that TRPM8 may control AMPK activity thus modulating cellular autophagy to regulate the proliferation and migration of breast cancer cells. In this study, overexpression of TRPM8 enhanced the level of basal autophagy, whereas TRPM8 knockdown reduced the level of basal autophagy in several types of mammalian cancer cells. Moreover, the activity of the TRPM8 channel modulated the level of basal autophagy. The mechanism of regulation of autophagy by TRPM8 involves autophagy-associated signaling pathways for activation of AMPK and ULK1 and phagophore formation. Impaired AMPK abolished TRPM8-dependent regulation of autophagy. TRPM8 interacts with AMPK in a protein complex, and cytoplasmic C-terminus of TRPM8 mediates the TRPM8–AMPK interaction. Finally, basal autophagy mediates the regulatory effects of TRPM8 on the proliferation and migration of breast cancer cells. Thus, this study identifies TRPM8 as a novel regulator of basal autophagy in cancer cells acting by interacting with AMPK, which in turn activates AMPK to activate ULK1 in a coordinated cascade of TRPM8-mediated breast cancer progression.

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