Withdrawal from contact inhibition is necessary for epithelial cancer precursor cells to initiate cell growth and motility. Nevertheless, little is understood about the mechanism for the sudden initiation of cell growth under static conditions. We focused on cellular junctions as one region where breaking out of contact inhibition occurs. In well-differentiated endometrial cancer cells, Sawano, the ligand administration for tricellular tight junction protein LSR, which transiently decreased the robust junction property, caused an abrupt increase in cell motility and consequent excessive multilayered cell growth despite being under contact inhibition conditions. We observed that macropinocytosis essentially and temporarily occurred as an antecedent event for the above process at intercellular junctions without disruption of the junction apparatus but not at the apical plasma membrane. Collectively, we concluded that the formation of macropinocytosis, which is derived from tight junction-mediated signaling, was triggered for the initiation of cell growth in static precancerous epithelium.

中文翻译：

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LSR 从三细胞角的易位导致细胞-细胞界面处的巨胞饮作用，作为打破接触抑制的触发因素

退出接触抑制对于上皮癌前体细胞启动细胞生长和运动是必要的。然而，关于在静态条件下突然启动细胞生长的机制知之甚少。我们将细胞连接点作为突破接触抑制发生的一个区域。在分化良好的子宫内膜癌细胞中，三细胞紧密连接蛋白 LSR 的配体 Sawano 会暂时降低稳健连接特性，导致细胞运动突然增加，从而导致细胞过度生长，尽管处于接触抑制条件下。我们观察到，巨胞饮作用在细胞间连接处作为上述过程的先导事件基本上和暂时发生，而没有破坏连接装置，但不是在顶端质膜处。总的来说，我们得出结论，巨胞饮作用的形成是由紧密连接介导的信号传导引起的，是为启动静态癌前上皮细胞生长而触发的。