Random Records

I have read the news and view in the nature which summarizes two articles demonstrating the tumor cells, esp. lung adenocarcinomas (advanced and aggressive stage) divided and gave rise to two cell populations. ( doi :10.1038/nature22494) 1. tumour cells - actively dividing cells 2. supporting cell or so called "niche cell" - which provide the microenvironment to support the growth of the tumour cells Picture indicates the tumour cell divides and gives rise to two subpopulations (a). Within the tumour tissue, there are two cell subpopulations, one support the growth of tumour by which it secretes the growth factor that can stimulate the tumour cell growth (b). Question remains; supporting cell can secrete and promote the cancer growth in the other cancer type besides the its own neighbouring cells

Paper: The crosstalk between Wnt/beta-catenin signaling pathway with DNA damage response and oxidative stress: Implications in cancer therapy (doi:10.1016/j.dnarep.2017.01.003) Before that we thought wnt signaling might not be related to DNA repair pathway, at all. Then we find this paper writing the review of wnt signaling contributing to DNA damage response and a bit of DNA repair. wnt signaling: 1. control gene expression 2 cell polarity 3. cell adhesion 4. cell behavior 5. DNA damage response --- Oxidative stress affect the wnt signaling, oxidative stress can cause the DNA lesion --- scope of this paper; review on the crosstalk of DDR, DNA repair, cellular activities through the wnt signaling pw. DDR: 1. sense the damage 2. transduce the signal to effector 3. determine the cell fate; cell cycle, fix, or death wnt signaling 1. determine the cell fate 1.1 cell proliferation 1.2  apoptosis 2. induce DDR through various protein 2.1 H2Ax 2.2 p16-INK4...

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...