Autophagy the membrane precursors (Mizushima et al., 2002).

Autophagy iSM1 s
one of the natural programmed cell death, which functions as a destructive
mechanism of cell death that dissociates unwanted or dysfunctional components.
This process prevents accumulation of damaged organelles (Mizushima & Komatsu, 2011) and recycles the cellular components
in extreme cases of starvation of cells (Kobayashi, 2015). Autophagy is mediated through four
pathways that are macroautophagy, microautophagy, chaperone-mediated autophagy,
and finally mitophagy. Macroautophagy is the major pathway of autophagy that
involves formation of autophagosome from the membrane precursors (Mizushima et al., 2002). Autophagosome
are then lysed by the lysosome and the components are degraded into smaller
pieces (Mizushima & Komatsu, 2011). In microautophagy, the lysosome
will engulf cytoplasmic organelles into 
lysosome (Mizushima et al., 2002) through inward invagination (Hafner ?esen et al., 2012). Meanwhile, chaperone-mediated autophagy (CMA) involves the chaperone
complex to bind with cytosolic proteins and later send to lysosome for
degradation (Bandyopadhyay et al., 2008).
Cytosolic proteins bind to the monomeric lysosome-associated membrane protein
type 2A (LAMP-2A) which found on the lysosomal membrane and perform
translocation to lysosome after formation of LAMP-2A complex (Mizushima & Komatsu, 2011). Lastly, the fourth autophagy pathway
is mitophagy, the mediation of mitochondria dissociation from the environmental
stress regardless of the condition of mitochondria (Youle & Narendra, 2010).Anoikis,
a Greek word meaning the state of homelessness, is a kind of apoptosis due to
the detachment of cells from the surrounding  ECMSM1  (Frisch & Francis, 1994). In general, ECM is composed of extracellular
molecules secreted by cells that provide support, segregate tissues from one
another, and regulate intercellular communication to the surrounding cells (Alberts, 2017). In addition to enabling localization
of cells to the ECM, anoikis also helps to promote cancer cell death and
inhibit further cancer cell proliferation (Gilmore, 2005; Xiaolin
Zhang & Yu, 2016).  

The
mechanism of anoikis is similar to both intrinsic and extrinsic pathways in
cancer cells, with the added condition of detachment from ECM (Gilmore,
2005). Numerous Bcl-2 family
members that are involved in both apoptotic pathway have been identified to
regulate anoikis (Paoli et al., 2013). Based on previous study,
BH3-only pro-apoptotic proteins, a subset of Bcl-2 family, were found to be
involved in the intrinsic anoikis cascade (Bouillet
& Strasser, 2002). Members of BH3-only
pro-apoptotic proteins include Bid and Bim. The activated Bid and Bim will then
act as activators when cells detach from ECM followed by the Bax-Bak oligomer
formation (R.
C. Taylor et al., 2008). When cells are not anchored to the ECM, it
induces the release of Bim proteins which translocate into the mitochondria.
This can lead to the aggregation of Bim protein that will inhibit the cell proliferation
and induce protein degradation.

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miRNAs
are small and conserved non-coding RNA that interrupt the synthesis of proteins
through RNA silencing. RNA silencing happens when the miRNA-protein complex
known as RNA-induced silencing complex (RISC) cleaves the mature mRNA strand by
binding to the complementary strand of it (MacFarlane & Murphy, 2010). miRNA regulation of genes are known
to be complex, as one miRNA is capable of targeting many mRNAs (Lim et al., 2005), while many
miRNAs are capable of targeting a single mRNA (Krek et al., 2005).

However,
dysregulation of miRNA showed the six hallmarks of cancer either in an oncogenic
or tumour suppressive way SM1 (Peng
& Croce, 2016). Oncogenic miRNA are the
viable miRNA that can control constitutive cancer cell proliferation and induce
the formation of tumour or to resist cancer cell death, such as apoptosis. This
uncontrollable division of cells is cancerous and may be fatal (Peng
& Croce, 2016). On the other hand, tumour
suppressive miRNA refer to the miRNA that are unable to promote malignancy
tumorigenesis (Osborne et al., 2004). Tumour suppressive miRNA suppress
both the formation of tumour and metastasis. Viability of cancer cells are
usually decreased and eventually undergo cell death (Lynch &
Rustgi, 2012).

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