To investigate the effects of TGF-β1 on the proliferation and apoptosis of cervical cancer Hela cells in vitro. Human cervical cancer Hela cells were cultured in vitro and divided into the experimental and control groups. In the experimental groups, Hela cells were stimulated with different concentrations of TGF-β1 (0.01, 0.1, 1, and 10 ng/mL), while Hela cells cultured in serum-free medium without TGF-β1 were used as controls. The CCK8 method was adopted to detect the effect of TGF-β1 on Hela cell proliferation, and flow cytometry was used to determine cell apoptosis 72 h after TGF-β1 treatment. Compared with the control group, the CCK-8 tests showed that different concentrations of TGF-β1 had no obvious effect on Hela cell proliferation 24 h after treatment (P > 0.05). However, upon 48 or 72 h of treatment, TGF-β1 significantly inhibited the proliferation of Hela cells in a time- and dose-dependent manner (P < 0.05). The flow cytometry results indicated that TGF-β1 influenced the apoptosis of human cervical cancer Hela cells in a dose-dependent manner after 72 h of treatment (P < 0.05). TGF-β1 significantly inhibited the growth and induced the apoptosis of human cervical Hela cells in vitro.
Symmetric cell division (SD) and asymmetric cell division (ASD) were the unique characteristics of stem cells and the mechanisms underlying stem cell renewal. While recent studies have identified the presence of SD and ASD in lung cancer stem cells (CSCs), the mechanisms regulating SD and ASD in cancer state have not been elucidated, mostly due to the lack of stable cellular models of SD and ASD in CSC research. In this study, the interaction between Zeb1, an Epithelial-Mesenchymal Transition (EMT) factor shown to regulate CSCs self-renew, and Numb, which regulates SD and ASD in the normal neural stem cell was investigated using the stable mouse Lewis lung adenocarcinoma SD (LLC-SD) and ASD (LLC-ASD) lines established from our previous study. The most significant finding derived from this line of research is that we have identified and molecularly ordered the axis of Zeb1-miR-31-Numb that regulates the SD, a mechanism of CSC self-renewal that has not been previously described. More specifically, the expression of Zeb1 and Numb were both significantly higher in LLC-SD than LLC-ASD cells. Silencing of Zeb1 or Numb expression lead to decreased ratio of SD and weakened single-cell cloning formation, tumor growth and tumor metastasis, respectively. The rescure experiments have molecularly ordered the regulation of Numb by Zeb1, indirectly mediated by miR-31. Moreover, we also provided preliminary evidence supporting the clinical relevance of our finding. In summary, our study provides a new insight for the self-renew of lung CSCs in which SD is regulated by the axis of Zeb1-miR-31-Numb.
The paper proposes several mathematical models of the multidirectional associative memory (MAM) neural network by analyzing its structure. A model of MAM with distributed delays is studied. Under some new assumptions on activation functions, 2 n 0 [m/2] invariant subsets of MAM are constructed. Then the existence and the exponential stability of 2 n 0 [m/2] periodic solutions located on invariant subsets are obtained by constructing a suitable Liapunov function and a Poincaré mapping. An estimating method of the exponential convergence rate is given. The obtained results are new to MAM neural networks. An example is given to illustrate the effectiveness of the results.
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