Dahiya Neetu
Laboratory of Molecular Biology & Immunology, NIH, Baltimore, MD 21224, USA.
Center for Biologics Evaluation & Research, US Food & Drug Administration, Silver Spring, MD 20993, USA.
Future Sci OA. 2020 Mar 16;6(4):FSO457. doi: 10.2144/fsoa-2019-0123.
In our previous report, we identified roles of CLDN7 in regulation of cell signaling. The goal of this study was to identify proteins interacting with CLDN7 in ovarian cancer.
The yeast two-hybrid system was used to identify proteins directly interacting with CLDN7 and cell survival was tested using colony formation assay.
Amyloid precursor-like protein 2 (APLP2) was found directly associated with CLDN7 in ovarian cancer cell line OVCA420. In addition, APLP2 showed increased expression in ovarian cancer cell lines and tumor tissue samples compared with non-neoplastic ovarian tissues. Knockdown of CLDN7 led to increased expression of APLP2 at both the mRNA and protein levels. Knockdown of APLP2 was associated with decreased cell survival in ovarian cancer cells.
We show a direct interaction of CLDN7 with APLP2. These findings suggest novel regulatory role for APLP2 in ovarian cancer, a role that appears to be mediated by CLDN7.
在我们之前的报告中，我们确定了CLDN7在细胞信号调节中的作用。本研究的目的是鉴定在卵巢癌中与CLDN7相互作用的蛋白质。
使用酵母双杂交系统鉴定与CLDN7直接相互作用的蛋白质，并使用集落形成试验检测细胞存活率。
在卵巢癌细胞系OVCA420中发现淀粉样前体样蛋白2（APLP2）与CLDN7直接相关。此外，与非肿瘤性卵巢组织相比，APLP2在卵巢癌细胞系和肿瘤组织样本中的表达增加。CLDN7的敲低导致APLP2在mRNA和蛋白质水平上的表达增加。APLP2的敲低与卵巢癌细胞存活率降低有关。
我们展示了CLDN7与APLP2的直接相互作用。这些发现表明APLP2在卵巢癌中具有新的调节作用，这一作用似乎由CLDN7介导。
