Originally it was believed that autophagy in cancer
cells had tumor-suppression mechanism i.e. an anti-tumor mechanism. This belief
was derived from early reports that the essential autophagy
gene ATG6/BECN1 was monoallelically lost in 40% to 75% of human
prostate, breast, and ovarian cancers (13–15).

This
hypothesis was consequential from the observations that autophagy deficiency in
mice results in benign hepatomas (18)  This also suggests that
autophagy may be required for transformation from a benign to a malignant form.

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Some mechanisms by which this could result have been identified but solid proof
that any of this occur in human cancers is still lacking. (Eileen White ).

There are a few proposed mechanisms by which autophagy
may suppress tumorigenesis. (12). Deficiency of ATG7, BECN1 or ATG5 (thought to
be tumor-suppressing) result in an elevated p63 accumulation, mitochondrial
defects, oxidative stress, DNA damage and cell death. This leads to chronic
tissue damage, inflammation, oncogenic signaling, genome instability and
eventually tumor initiation. Suggested mechanisms by which autophagy instead
promotes tumor growth, is increased autophagy due to deregulated proliferation,
leading to decreased p53, oxidative stress, ER stress, as well as increased
mitochondrial function, metabolism and stress tolerance. 

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