Pdlim7 is made of an N-terminal PDZ domain and three C-terminal LIM domains. The PDZ domain interacts with actin-binding proteins. Its LIM domains bind to proteins involved in mitogenic or insulin signaling such as receptor tyrosine kinases (Jennifer Krcmery et al. 2010).
When PDZ-LIM proteins do not function well, they can promote tumor growth and malignant transformation. In one study, Pdlim7 played a role in tumorigenesis in a mechanism by triggering mitosis and decreasing p53 antiproliferative activity (Cho-Rok Jung et al. 2010). Kaplan-Meier survival analysis showed that the expression level of Pdlim7 is related to the survival rate of breast cancer patients. Also, PDZ domain could interact with human papillomaviruses, which is related to cervical cancer (Kazunori Nagasaka et al. 2013). HPV-induced cancer cells often have viral sequences integrated into the cellular DNA.
Additionally, Pdlim7 produces multiple alternatively spliced mRNA variants, two of which include a unique terminal exon.
Additionally, Pdlim7 produces a slice variant.
Materials and Methods
In this study, 6 cell lines were used: MDA-MB_231, MDA-MB-468, MCF-7, T47-D, MDA-MB-435(breast cancer cells) and HeLa cells( cervical cancer cells).
RT-PCR was performed using specifically designed primers. One pair only amplified the splice variant with long terminal exon (arrows in Fig.1 and Fig.3). Another pair only amplified the splice variant with exon 8 (arrows in Fig.2 and Fig.3). GAPDH was used as the housekeeping control. Samples with no templates were used as negative template control.
RT-PCR products were visualized on 1.0 % agarose gels. PCR products were purified using QIAquick® PCR Purification Kit. Purified PCR products were sequenced by GENEWIZ® and were confirmed by BLAST.
This study demonstrated that the Pdlim7 gene produces splice variants with the unique terminal exon that only highly expressed in HeLa cells, but not in breast cancer cells.
In this study, the Pdlim7 gene produced a splice variant with the unique terminal exon only in HeLa cells but not in breast cancer cells. Different types of cancer might utilize specific Pdlim7 translation products as scaffolding proteins to facilitate the production different signaling complexes.
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