Cancer is a leading cause of death worldwide, accounting for 8.2 million deaths (around 13% of all deaths) in 2012, with this number expected to rise to over 11 million by 2030 (1). The term “cancer” groups over 100 distinct diseases that share a series of “acquired capabilities,” which were first defined by Hanahan and Weinberg in 2000 consisting of six hallmark alterations in cell physiology that collectively dictate malignant growth: cell sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of programmed cell death, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis (2). In the last 25 years, the description and interpretation of genomic abnormalities in cancer cells have dominated cancer research (3). However, bioinformatic analyses suggest that cancer-related driver mutations affect a dozen or more core cell signaling pathways (4), suggesting that individual targets will not be fruitful candidates for therapeutic development, and instead, intervening with cellular processes will be more effective. In this regard, it has become increasingly clear that many key oncogenic signaling pathways that support tumor cell growth and survival converge at cell metabolism (5). In fact, the reprogramming of energy metabolism, which relies on mitochondrial function, is absolutely required for malignant transformation, and for this reason, it has recently been added as a hallmark of cancer (6). This research topic focuses on the role of the endoplasmic reticulum (ER)-to-mitochondria communication in the regulation of mitochondrial function, with special emphasis on Ca2+ transfer, and its impact on cancer cell fate.
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|Titolo:||Editorial: Inter-Organelle Calcium Communication in Cancer|
|Data di pubblicazione:||2018|
|Appare nelle tipologie:||03.1 Articolo su rivista|