Programmed cell death (PCD), referring to apoptosis, autophagy and programmed necrosis, is proposed to be death of a cell in any pathological format, when mediated by an intracellular program. These three forms of PCD may jointly decide the fate of cells of malignant neoplasms; apoptosis and programmed necrosis invariably contribute to cell death, whereas autophagy can play either pro-survival or pro-death roles. Recent bulk of accumulating evidence has contributed to a wealth of knowledge facilitating better understanding of cancer initiation and progression with the three distinctive types of cell death. To be able to decipher PCD signalling pathways may aid development of new targeted anti-cancer therapeutic strategies. Thus in this review, we present a brief outline of apoptosis, autophagy and programmed necrosis pathways and apoptosis-related microRNA regulation, in cancer. Taken together, understanding PCD and the complex interplay between apoptosis, autophagy and programmed necrosis may ultimately allow scientists and clinicians to harness the three types of PCD for discovery of further novel drug targets, in the future cancer treatment.

/pdf/programmed-cell-death-pathways-in-cancer-a-review-of-3uzhx02ea0.pdf

Programmed cell death pathways in cancer: a review of apoptosis, autophagy and programmed necrosis

Reactive oxygen species and cancer paradox: To promote or to suppress?

Selenium compounds as therapeutic agents in cancer

Aging is a complex phenomenon and its impact is becoming more relevant due to the rising life expectancy and because aging itself is the basis for the development of age-related diseases such as cancer, neurodegenerative diseases and type 2 diabetes. Recent years of scientific research have brought up different theories that attempt to explain the aging process. So far, there is no single theory that fully explains all facets of aging. The damage accumulation theory is one of the most accepted theories due to the large body of evidence found over the years. Damage accumulation is thought to be driven, among others, by oxidative stress. This condition results in an excess attack of oxidants on biomolecules, which lead to damage accumulation over time and contribute to the functional involution of cells, tissues and organisms. If oxidative stress persists, cellular senescence is a likely outcome and an important hallmark of aging. Therefore, it becomes crucial to understand how senescent cells function and how they contribute to the aging process. This review will cover cellular senescence features related to the protein pool such as morphological and molecular hallmarks, how oxidative stress promotes protein modifications, how senescent cells cope with them by proteostasis mechanisms, including antioxidant enzymes and proteolytic systems. We will also highlight the nutritional status of senescent cells and aged organisms (including human clinical studies) by exploring trace elements and micronutrients and on their importance to develop strategies that might increase both, life and health span and postpone aging onset.

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence.

The cellular response to survive or to undergo death is fundamental to the benefit of the organism, and errors in this process can lead to autoimmunity and cancer. The transcription factor nuclear factor κB (NF-κB) functions to block cell death through transcriptional induction of genes encoding anti-apoptotic and antioxidant proteins. This is essential for survival of activated cells of the immune system and for cells undergoing a DNA damage response. In Ras-transformed cells and tumors as well as other cancers, NF-κB functions to suppress apoptosis--a hallmark of cancer. Critical prosurvival roles for inhibitor of NF-κB kinase (IKK) family members, including IKKe and TBK1, have been reported, which are both NF-κB-dependent and -independent. While the roles of NF-κB in promoting cell survival in lymphocytes and in cancers is relatively clear, evidence has been presented that NF-κB can promote cell death in particular contexts. Recently, IKK was shown to play a critical role in the induction of autophagy, a metabolic response typically associated with cell survival but which can lead to cell death. This review provides an historical perspective, along with new findings, regarding the roles of the IKK and NF-κB pathways in regulating cell survival.

Regulation of cell death and autophagy by IKK and NF-κB: critical mechanisms in immune function and cancer.

Autophagy can protect cells while also contributing to cell damage, but the precise interplay between apoptosis and autophagy and the contribution of autophagy to cell death are still not clear. Previous studies have shown that supranutritional doses of sodium selenite promote apoptosis in human leukemia NB4 cells. Here, we report that selenite treatment triggers opposite patterns of autophagy in the NB4, HL60, and Jurkat leukemia cell lines during apoptosis and provide evidence that the suppressive effect of selenite on autophagy in NB4 cells is due to the decreased expression of the chaperone protein Hsp90 (heat shock protein 90), suggesting a novel regulatory function of Hsp90 in apoptosis and autophagy. Excessive or insufficient expression indicates that Hsp90 protects NB4 cells from selenite-induced apoptosis, and selenite-induced decreases in the expression of Hsp90, especially in NB4 cells, inhibit the activities of the IκB kinase/nuclear factor-κB (IKK/NF-κB) signaling pathway, leading to less nuclear translocation and inactivation of NF-κB and the subsequent weak binding of the becn1 promoter, which facilitates the transition from autophagy to apoptosis. Taken together, our observations provide novel insights into the mechanisms underlying the balance between apoptosis and autophagy, and we also identified Hsp90-NF-κB-Beclin1 as a potential biological pathway for signaling the switch from autophagy to apoptosis in selenite-treated NB4 cells.

Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells

The p38 MAPK-regulated PKD1/CREB/Bcl-2 pathway contributes to selenite-induced colorectal cancer cell apoptosis in vitro and in vivo.

Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis.

Corrigendum to “Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis” [Cancer Lett. 315 (1) (2012) 78–85]

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Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells

The p38 MAPK-regulated PKD1/CREB/Bcl-2 pathway contributes to selenite-induced colorectal cancer cell apoptosis in vitro and in vivo.

Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis.

Corrigendum to “Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis” [Cancer Lett. 315 (1) (2012) 78–85]