Inositol 1, 4, 5-trisphosphate-dependent nuclear calcium signals regulate angiogenesis and cell motility in triple negative breast cancer

Autor: Clarissa Coelho de Carvalho, Márcio Flávio Dutra Moraes, Gabriel Fernandes, M. Fatima Leite, Carlos Alberto Gonçalves, Puebla Cassini, Ana Cândida Araújo e Silva, Barbara Hissa, Matheus de Castro Fonseca, Brígida Gomes Almeida, José Miguel Ortega, André G. Oliveira, Lucíola S. Barcelos, Andressa França, Luciana E. Drumond, Erika S. Guimarães, Rodrigo Matta Machado, Marina De Brot
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Adenoviruses
Angiogenesis
Physiology
Tumor Physiology
Cancer Treatment
lcsh:Medicine
Gene Expression
Triple Negative Breast Neoplasms
Inositol 1
4
5-Trisphosphate
Cardiovascular Physiology
Pathology and Laboratory Medicine
Mice
Cell Movement
Breast Tumors
Basic Cancer Research
Medicine and Health Sciences
lcsh:Science
Triple-negative breast cancer
Mice
Inbred BALB C
Multidisciplinary
Neovascularization
Pathologic
Chemistry
Cell migration
Primary tumor
Gene Expression Regulation
Neoplastic
Cell Motility
Oncology
Medical Microbiology
Tumor Angiogenesis
Viral Pathogens
Viruses
Heterografts
Female
Pathogens
Research Article
medicine.medical_specialty
Motility
Microbiology
Focal adhesion
03 medical and health sciences
Downregulation and upregulation
Internal medicine
Cell Line
Tumor
Breast Cancer
medicine
Genetics
Animals
Humans
Calcium Signaling
Microbial Pathogens
Cell Proliferation
Cell Nucleus
lcsh:R
Organisms
Cancers and Neoplasms
Biology and Life Sciences
Cell Biology
medicine.disease
Chemokine CXCL10
030104 developmental biology
Endocrinology
Tumor progression
Cancer research
lcsh:Q
DNA viruses
Developmental Biology
Zdroj: PLoS ONE
PLoS ONE, Vol 12, Iss 4, p e0175041 (2017)
ISSN: 1932-6203
Popis: Increases in nuclear calcium concentration generate specific biological outcomes that differ from those resulting from increased cytoplasmic calcium. Nuclear calcium effects on tumor cell proliferation are widely appreciated; nevertheless, its involvement in other steps of tumor progression is not well understood. Therefore, we evaluated whether nuclear calcium is essential in other additional stages of tumor progression, including key steps associated with the formation of the primary tumor or with the metastatic cascade. We found that nuclear calcium buffering impaired 4T1 triple negative breast cancer growth not just by decreasing tumor cell proliferation, but also by enhancing tumor necrosis. Moreover, nuclear calcium regulates tumor angiogenesis through a mechanism that involves the upregulation of the anti-angiogenic C-X-C motif chemokine 10 (CXCL10-IP10). In addition, nuclear calcium buffering regulates breast tumor cell motility, culminating in less cell invasion, likely due to enhanced vinculin expression, a focal adhesion structural protein. Together, our results show that nuclear calcium is essential for triple breast cancer angiogenesis and cell migration and can be considered as a promising strategic target for triple negative breast cancer therapy.
Databáze: OpenAIRE
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