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

Thishypothesis was consequential from the observations that autophagy deficiency inmice results in benign hepatomas (18)  This also suggests thatautophagy may be required for transformation from a benign to a malignant form.Some mechanisms by which this could result have been identified but solid proofthat any of this occur in human cancers is still lacking. (Eileen White ). There are a few proposed mechanisms by which autophagymay suppress tumorigenesis.

(12). Deficiency of ATG7, BECN1 or ATG5 (thought tobe tumor-suppressing) result in an elevated p63 accumulation, mitochondrialdefects, oxidative stress, DNA damage and cell death. This leads to chronictissue damage, inflammation, oncogenic signaling, genome instability andeventually tumor initiation.

Suggested mechanisms by which autophagy insteadpromotes tumor growth, is increased autophagy due to deregulated proliferation,leading to decreased p53, oxidative stress, ER stress, as well as increasedmitochondrial function, metabolism and stress tolerance. 

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