Metabolic Regulation of Caspase 2 in Breast Cancer

2009 ◽  
Author(s):  
Marisa Buchakjian
Keyword(s):  
Breast Cancer ◽  
Metabolic Regulation ◽  
Caspase 2

The Regulatory Role of Both MBNL1 and MBNL1-AS1 in Several Common Cancers

2021 ◽  
Vol 27 ◽  
Author(s):  
Qi Zhang ◽  
Yinxin Wu ◽  
Jinlan Chen ◽  
Yuxuan Cai ◽  
Bei Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Colorectal Cancer ◽  
Gastric Cancer ◽  
Lung Cancer ◽  
Overall Survival ◽  
Survival Rate ◽  
Rna Splicing ◽  
Metabolic Regulation ◽  
Overall Survival Rate

Background: MBNL1, a protein encoded by q25 gene on chromosome 3, belongs to the tissue-specific RNA metabolic regulation family, which controls RNA splicing.[1]MBNL1 formed in the process of development drive large transcriptomic changes in cell differentiation,[2] it serves as a kind of tumor differentiation inhibitory factor.MBNL1 has a close relationship with cancer, comprehensive analysis, [3]found that breast cancer, leukemia, stomach cancer, esophageal adenocarcinoma, glial cell carcinoma and another common tumor in the cut, and cut in Huntington's disease. But MBNL1 plays a promoting role in cervical cancer, is contradictory in colorectal cancer, It promotes colorectal cancer cell proliferation, On the other hand, it inhibits its metastasis, so it is an important physiological marker in many cancers. When we integrated the role of MBNL1 protein in various tumors, we found that its antisense RNA, MBNL1-AS1, had a good inhibitory effect in several colorectal cancer, non-small cell lung cancer, and gastric cancer. Objective: To elucidate the expression of MBNL1 and MBNL1-AS1 in various tumors, and to search for their physiological markers. Methods: It was searched by the PUMUB system and summarized its expression in various cancers. Results: MBNL1 was down-regulated, leukemia, breast cancer, glioblastoma, gastric cancer, overall survival rate, recurrence, metastasis increased. While the metastasis of colon cancer decreased, proliferation was promoted, and the effect of both was promoted for cervical cancer.MBNL1-AS1 was down-regulated, and the overall survival rate, recurrence, and metastasis of lung cancer, colorectal cancer, and bladder cancer increased. Conclusion: MBNL1 may be an important regulator of cancer, and MBNL1-AS1 is a better tumor suppressor.

SUMOylation involves in β-arrestin-2-dependent metabolic regulation in breast cancer cell

2020 ◽  
Vol 529 (4) ◽  
pp. 950-956
Author(s):  
Changsheng Dong ◽  
Ying Li ◽  
Qun Niu ◽  
Houshun Fang ◽  
Jie Bai ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Metabolic Regulation

scholarly journals Epigenetic and metabolic regulation of breast cancer stem cells

2015 ◽  
Vol 16 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Hui-xin Liu ◽  
Xiao-li Li ◽  
Chen-fang Dong
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Metabolic Regulation ◽  
Breast Cancer Stem Cells

scholarly journals The landscape of tiered regulation of breast cancer cell metabolism

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Rotem Katzir ◽  
Ibrahim H. Polat ◽  
Michal Harel ◽  
Shir Katz ◽  
Carles Foguet ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Metabolic Regulation ◽  
Cell Metabolism ◽  
Cancer Cell Line ◽  
Hierarchical Organization ◽  
Metabolic Reprogramming ◽  
A Genome ◽  
Cancer Cell Metabolism

AbstractAltered metabolism is a hallmark of cancer, but little is still known about its regulation. In this study, we measure transcriptomic, proteomic, phospho-proteomic and fluxomics data in a breast cancer cell-line (MCF7) across three different growth conditions. Integrating these multiomics data within a genome scale human metabolic model in combination with machine learning, we systematically chart the different layers of metabolic regulation in breast cancer cells, predicting which enzymes and pathways are regulated at which level. We distinguish between two types of reactions, directly and indirectly regulated. Directly-regulated reactions include those whose flux is regulated by transcriptomic alterations (~890) or via proteomic or phospho-proteomics alterations (~140) in the enzymes catalyzing them. We term the reactions that currently lack evidence for direct regulation as (putative) indirectly regulated (~930). Many metabolic pathways are predicted to be regulated at different levels, and those may change at different media conditions. Remarkably, we find that the flux of predicted indirectly regulated reactions is strongly coupled to the flux of the predicted directly regulated ones, uncovering a tiered hierarchical organization of breast cancer cell metabolism. Furthermore, the predicted indirectly regulated reactions are predominantly reversible. Taken together, this architecture may facilitate rapid and efficient metabolic reprogramming in response to the varying environmental conditions incurred by the tumor cells. The approach presented lays a conceptual and computational basis for mapping metabolic regulation in additional cancers.

Quantitative proteome and lysine succinylome analyses provide insights into metabolic regulation in breast cancer

Breast Cancer ◽  
2018 ◽  
Vol 26 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Chenchen Liu ◽  
Ying Liu ◽  
Lei Chen ◽  
Mingjun Zhang ◽  
Wei Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metabolic Regulation

scholarly journals Caspase-2 is involved in cell death induction by taxanes in breast cancer cells

2013 ◽  
Vol 13 (1) ◽  
pp. 42 ◽  
Author(s):  
Michael Jelínek ◽  
Kamila Balušíková ◽  
Dana Kopperová ◽  
Vlasta Němcová-Fürstová ◽  
Jan Šrámek ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Caspase 2

scholarly journals Energetic regulation of coordinated leader–follower dynamics during collective invasion of breast cancer cells

2019 ◽  
Vol 116 (16) ◽  
pp. 7867-7872 ◽  
Author(s):  
Jian Zhang ◽  
Kayla F. Goliwas ◽  
Wenjun Wang ◽  
Paul V. Taufalele ◽  
Francois Bordeleau ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Energy Level ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Breast Cancer Cells ◽  
Metabolic Regulation ◽  
Collective Behaviors ◽  
Cellular Energy ◽  
Collective Invasion ◽  
Leader Cell

The ability of primary tumor cells to invade into adjacent tissues, followed by the formation of local or distant metastasis, is a lethal hallmark of cancer. Recently, locomoting clusters of tumor cells have been identified in numerous cancers and associated with increased invasiveness and metastatic potential. However, how the collective behaviors of cancer cells are coordinated and their contribution to cancer invasion remain unclear. Here we show that collective invasion of breast cancer cells is regulated by the energetic statuses of leader and follower cells. Using a combination of in vitro spheroid and ex vivo organoid invasion models, we found that cancer cells dynamically rearrange leader and follower positions during collective invasion. Cancer cells invade cooperatively in denser collagen matrices by accelerating leader–follower switching thus decreasing leader cell lifetime. Leader cells exhibit higher glucose uptake than follower cells. Moreover, their energy levels, as revealed by the intracellular ATP/ADP ratio, must exceed a threshold to invade. Forward invasion of the leader cell gradually depletes its available energy, eventually leading to leader–follower transition. Our computational model based on intracellular energy homeostasis successfully recapitulated the dependence of leader cell lifetime on collagen density. Experiments further supported model predictions that decreasing the cellular energy level by glucose starvation decreases leader cell lifetime whereas increasing the cellular energy level by AMP-activated kinase (AMPK) activation does the opposite. These findings highlight coordinated invasion and its metabolic regulation as potential therapeutic targets of cancer.

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