Apoptosis

inhibit receptor aggregation, prevented curcumin-induced cell death (Bush JA, Cheung KJ, Jr, Li G 2002). Apoptosis in nasopharyngeal carcinoma cell line NCE induced by curcumin was found to up-regulate the Fas receptor gene as well as the protein in a dose-dependent manner (Yang FW, Huang JZ, Lin XL, Zhen ZN, Chen XM2005). Curcumin is able to inhibit the proliferation of CA46 cells and induce apoptosis by down-regulating the expression of c-myc, Bcl-2, and mutant-type p53, and up-regulating the expression

old cells with new ones, or may result from factors such as disease, localized injury, or even death of the whole organism. Apoptosis vs. Necrosis Apoptosis is a form of cell death that is caused by normal processes of the human body, necrosis on the other hand is a form of cell death that is caused by disease states or external inputs such as infection or injury. Apoptosis also known as programmed cell death may also be used as a defence mechanism for the body in the healing process and is usually

advances in cancer research is the idea of apoptosis and the genes that control it, where they have a profound effect on the malignant phenotype. P53 was the first tumor suppressor gene linked to apoptosis. Mutations in this tumor suppressor gene occur in the majority of human tumors and are often associated with advanced tumor stage and poor patient prognosis. Studies using p53 knockout mice demonstrated that endogenous p53 could participate in apoptosis. Also, it is now known that a lot of factors

Given the vital role of caspase activation in apoptotic cell death, blocking their function is a useful approach to find out whether apoptosis has a causal effect in triggering compensatory proliferation. In various species tissue regeneration was impaired if cell death was blocked with pan-caspase or effector caspase inhibitors (Fan and Bergmann 2008; Li et al. 2010; Ryoo and Bergmann 2012; Tseng et al. 2007). This approach has also been shown to ameliorate loss of neuronal cells and function after

Annexing V FITIC/PI was used to detect for the involvement of apoptosis based upon externalization of phospholipid phosphatidylserine (PS) and permeabilization of nuclear membrane for staining with PI. PS is a biomarker of early apoptotic stage, Annexin V has specific and high affinity for the anionic PS, when PS is exposed on cell surface Annexing V binds to it. PS indicates intermediate stages of apoptosis. Caspases-3 activation, nuclear fragmentation and mitochondrial membrane flux preceded PS

1.2.2. Mitochondrial pathway The mitochondrial pathway, also called intrinsic pathway, because it is initiated from inside the cell. Various stimuli such as growth factors withdrawal, DNA-damage, hypoxia, and oxidative stress can induce apoptosis through this cascade. These insults cause increasing permeability of the outer mitochondrial membrane and opening of the mitochondrial permeability transition (MPT) pore which is controlled by members of the Bcl-2 family proteins. This large family of proteins

Phosphorylation is the formation of a high-energy bond between a phosphate group and a target molecule in the presence of an enzyme. In a cellular environment, it is estimated that 1/10th to half of the total proteins are phosphorylated to perform a specific function in the cell. The concept of protein phosphorylation was first introduced by Edmond Fischer and Edwin Krebs in the year 1955, where they elucidated the necessity of ATP and a kinase (Known then as “converting enzyme”). Interestingly,

MITOCHONDRIAL MORPHOLOGY AND APOPTOSIS Mitochondrial morphology is found to be closely associated with apoptosis. It can be found linked to mitochondrial fragmentation which is concurrent with cytochrome c release during early stages of apoptosis facillated by Drp1 recruitment to mitochondria(4). It has been shown that RNAi knockdown of fission proteins Fis1 as well Drp1 will not only prevent fragmentation of mitochondria but also prevents cell from triggering apoptosis by inhibiting cytochrome c release

constrain initiation and the development of different type of cancers (31) which make them proper candidate for cancer immunotherapy. It is also evident that probiotics are able to inhibit proliferation of mammalian cells in vitro (32) via induction of apoptosis by secreting safe, effective and natural substances and secretory compounds (28). Based on the above facts, the inhibitory effect of MVs derived from L. rhamnosus was evaluated on hepG2 cell line. In addition, to the best of our knowledge, current

significant effects on early stages (Stage I and stage II)39. The ST6Gal-I enzyme is reported to have three major functions in cancer progression. First, the α-2,6 sialylation can block the apoptosis mechanism40-41. Apoptosis is the mechanism of programmed cell death of multicellular organisms. The apoptosis process is induced by binding of cell galectins42-43. Galectins are a type of lectin and lectins are a class of proteins which can bind to specific proteins, via interacting with specific glycans