EMT/METs, both developmental and pathological, as being an
integral part of many related biological phenomena, e.g., the lineage diversification from pluripotent to uni-functional cells, cellular
reprogramming from a terminally differentiated fate back to a
pluripotent one, regulation of stem cell differentiation and maintenance, and plasticity in size and geometry in multicellular organization in response to contextual fluctuations, in all of which there
have been overwhelming evidence for mechanistic conservation
despite seeming phenomenological heterogeneity [11].
Taking such an optimistic view would mean that (1) more
EMT/MET models should be promoted because each can give us
a unique set of information applicable to all EMT/METs;
(2) understanding contextual details of any given EMT/MET
process is of paramount importance because such knowledge
would expedite parallel comparison of mechanistic insights gained
from different EMT/MET models; (3) each normal or disease
EMT/MET model, with its unique advantages and limitations,
should be compared with its closest “EMT/MET” relatives
because a limited number of EMT/MET contextual variations
would suggest the possibility of establishing an EMT/MET “phylogenetic tree”; and (4) most importantly, potential applications of
EMT/MET concept in cancer diagnosis and prevention can be
facilitated by integration of normal and disease EMT/MET
research.
In conclusion, we believe that a key element for conceptual
breakthroughs in EMT/MET research is to treat each partial
EMT/MET process as “an army of one,” with their unique cellular
history and tissue circumstance and ready to offer us mechanistic
insight of general importance. By doing so, we will be getting ever
closer to winning the battle to conquer cancer, the loftiest goal of
the EMT/MET research [12].
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