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I am not the signaling person but very curious to know how many cellular signaling do the cells have? Not so sure, every cell has all these pathways -- probably not I think..., -- Each pathway might have some molecules which interplays between the signal to response toward the stimuli (growth, stress, chemical, infection, etc.) correctly. 1.Akt Signaling Pathway 2.AMPK Signaling Pathway 3.Apoptosis Signaling Pathway 4.Estrogen Signaling Pathway 5.Insulin Signaling Pathway 6.JAK-STAT Signaling Pathway 7.MAPK Signaling Pathway 8.mTOR Signaling Pathway 9.NF-κB Signaling Pathway 10.Notch Signaling Pathway 11.p53 Signaling Pathway 12.TGF-β Signaling Pathway 13.Toll-like Receptor Signaling Pathway 14.VEGF Signaling Pathway 15.Wnt Signaling Pathway Ref: h ttps://www.tocris.com/signaling-pathways#.WD6R8FyoN0w

Note for: The Notch inhibitor cowanin accelerates nicastrin degradation (doi: 10.1038/s41598-018-23698-4) Notch alteration contributes to carcinogenesis. Therefore, it could be used as the target to treat the cancer. Using cell-based system to screen compound from Garcinia speciosa. 1/12 was found to inhibit notch signaling pw. HES1 and HES5 are the targets. Cowanin decreases HES1 and HES5 protein level. Cytotoxic to leukemic HPB-ALL. Notch signaling - many fundamental process; 1.proliferation 2.stem cell maintenance 3.differentiation (well just like wnt signaling pw) It is important for neuronal diff. It has been regulated through hairy and enhancer of split 1 ( HES1 ), HES5 and HES related ( HESR/HEY ) family genes. Aberration in Notch signaling participates in both multiple hematologic and solid malignancies. Notch signaling is activated by interaction between the ligand-expressing cell and the signal-receiving cell. Various Notch inhibitors; ...

Paper: Aberrant Wnt/beta-catenin signaling can induce chromosomal instability in colon cancer (doi:10.1073/pnas.0604206103) Abstract: Chromosomal instability (CIN+) 1. hallmark of most colon tumors 2. promote tumor progression by increasing rate of genetic aberration 3. occur from mitosis/spindle checkpoint defect Gap: Molecular mechanism is unk Rational: 1. colon cancer develop majorly from mutation of APC (Anaphase-promoting complex) 2. malfunction of APC causes wnt/b-catenin activation --> activate conductin/AXIN2 Research results: 1.wnt/catenin activation causes CIN via up-regulation of conductin 2.human colon cancer with CIN - found conductin higher 3.conductin is higher during the mitosis 4.conductin is localized with mitotic spindle of colon cancer cells 5.conductin binds polo-like kinase 1 6.when APC is forcibly downreglated by iRNA - conductin is ectopic upregulated lead to CIN in chromosomal stable colon cancer 7.higher expression of conductin di...