We can summarize it into two opposite pathways, depending on the presence of the intact LKB1-AMPK axis.
A detailed understanding of the molecular events occurring along opposite pathways will provide more comprehensive insight into the biology of estrogen-driven breast tumorigenesis in the case of mitochondrial genes and may have important implications for recommendations on treatment and risk-reduction strategies.
Both BMPrII and XAR1 (also known as xActRIIB) can act promiscuously to bind the ligands and type I receptors of the opposite pathways due to the high degree of sequence homology shared in protein interaction domains (Chang et al., 1997; Rejon et al., 2013).
The focus of this review to this point has been on EMT, however an important process that must be discussed is its "opposite" pathway, mesenchymal to epithelial transition (MET).
Analysis of the binding affinities for cross-pathway ligand-receptor interactions showed that there is less than a 10-fold difference in binding affinities for ligands to the receptors of the opposite pathway (Heinecke et al., 2009).
As proposed by Yegutkin et al. [ 66], an opposite pathway could lead to the recovery of adenine nucleotides, since adenylate kinase was identified as another key player in the metabolism of circulating ADP.
However, cell context and/or biochemical signaling, interaction with specific transcriptional partners and/or sub-cellular distribution of KLF6 could manage the outcome of KLF6 function to different and opposite tumor pathways.
On the contrary, a p17 variant derived from a Ugandan HIV-1 strain, named S75X, was found to trigger opposite signalling pathways, which induce B cell growth and malignant transformation.
Interestingly, considering the wavelength dependence of the light flicker, the two competing theories would predict opposite evolutionary pathways.
1– 3 Enantioconvergent processes are based on the transformation of a pair of enantiomers through opposite stereochemical pathways affecting retention and inversion of configuration.
The binding of TNF to TNFR can induce two opposite signaling pathways: one activates cell death process through the combination of TNFR I and FAS-associated death domain (FADD), leading to cell apoptosis; the other activates nuclear factor-kappa B (NF-kB) and c-Jun N-terminal kinase (JNK) through the combination of TNFR and TNFR-associated factors (TRAF), promoting cell survival and proliferation.
