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前期研究显示抑制LRP16的表达可以明显增加肿瘤细胞对辐射诱导凋亡的敏感性,但具体机制尚不清楚.大量研究表明,NF-κB信号通路在肿瘤产生辐射抵抗中起着重要的作用.为研究LRP16影响肿瘤细胞对辐射敏感性的可能机制,首先通过免疫荧光技术检测电离辐射刺激后不同时间点NF-κB的核转位情况;然后分别过表达和抑制LRP16的表达,采用Western印迹方法检测NF-κB在核蛋白与浆蛋白中的表达情况、IκB-α总体蛋白水平及磷酸化水平.结果发现,电离辐射后1 h,可见NF-κB明显入核;过表达LRP16可以促进NF-κB入核、提高IκB-α的磷酸化水平、促进IκB-α的降解;反之,抑制LRP16的表达可以抑制NF-κB入核、降低IκB-α的磷酸化水平、阻碍IκB-α的降解.上述研究结果表明,在HeLa细胞中LRP16可以影响电离辐射诱导的NF-κB核转位,该研究为LRP16参与肿瘤细胞产生辐射抵抗现象提供一种可能的机制.
Previous studies have shown that inhibition of LRP16 expression can significantly increase the sensitivity of tumor cells to radiation-induced apoptosis, but the exact mechanism is not clear.Numerous studies have shown that NF-κB signaling pathway plays an important role in tumor radiation response. To study the possible mechanism of LRP16 on the sensitivity of tumor cells to radiation, first detect the nuclear translocation of NF-κB at different time points by ionizing radiation after immunostaining; then overexpress and inhibit the expression of LRP16 respectively, and detect the expression of LRP16 by Western blot The expression of NF-κB in nucleoprotein and plasma protein, the level of IκB-αprotein and the level of phosphorylation of NF-κB were detected.It was found that NF-κB was marked into nucleus 1 hour after ionizing radiation.Overexpression of LRP16 could promote NF- Α, and promote the degradation of IκB-α. On the contrary, inhibiting the expression of LRP16 can inhibit the nuclear translocation of NF-κB, decrease the phosphorylation of IκB-α, and hinder the degradation of IκB-α. The results show that LRP16 can affect ionizing radiation-induced nuclear translocation of NF-κB in HeLa cells. This study provides a possible mechanism for LRP16 to participate in the phenomenon of radiation resistance in tumor cells .