ObjectiveTo understand research progress of influence of claudins on proliferation and activation for breast cancer. MethodThe relevant literatures of influence of claudins on proliferation and activation for breast cancer were retrieved and reviewed. ResultsThe claudins had 24 members in mammals,claudin-13 was missing in human beings.Expression and distribution mode of the claudins possessed highly tissue-specific,and multiple proteins were expressed in many organizations.The expressions of claudins could be regulated from the levels of transcription and post-transcription,coordinately regulated by the transcription factor and post-synthetic modifications.Claudins were related to epithelial-mesenchymal transition.Now the studies were relatively clear those focused on claudin-1,-2,-4,-6,and other subtypes,and the expression of claudin-1 indicated the poor prognosis of tumor;claudin-2 was closely related to liver metastasis of breast cancer;claudin-4 was closely related to triple negative breast cancer;the function of claudin-6 in the breast cancer was controversial.In addition to the claudins mentioned above,other claudin members also played certain roles in normal breast and malignant breast tumors.Claudin-5 might participate in metastasis of breast cancer through N-WASP and ROCK signal pathway;CD-24 and claudin-7 immunodepression had a certain guiding significance on prognosis of invasive ductal carcinoma;the expressions of claudin-16 and HAPLN3 gene were remarkably increased in human breast cancer;Claudin-20 induced breast cancer cells into a subtype that possessed the high invasiveness and weakened the resis-tance of epithelial-mesenchymal transition.Recently,the claudin-low subtype was proposed,and it differed from other types of breast cancer in many aspects,and also it had a better prognosis than other types of triple negative breast cancer. ConclusionsClaudin,being an important member of tight junction protein,is confirmed to be related to epithelial-mesenchymal transition.Claudins play important roles in dissociaton,activation,invasiveness,and metastasis of breast cancer,but there is no final conclusion which member contributes to invasiveness and metastasis of breast cancer.Moreover,there are opposite conclusions on some certain claudins members in breast cancer which might due to the different subtypes of breast cancer,so,further studies about the function of claudins in different subtypes are needed eagerly.
Objective To study the effect of down-regulation of Claudin-3 mediated by adeno-associated virus (AAV) of shRNA on the cultured retinal ganglion cells (RGCs) in vitro. Methods RGCs isolated from mouse eyes were divided into normal control group, AAV-shScramble group, and AAV-shClaudin-3 group. The RGCs in AAV-shScramble group and AAV-shClaudin3 group were treated with AAV-shScramble and AAV-shClaudin-3 respectively 24 hours after cell seeding. Dynamic live cell fluorescence microscopy was used to observe the transfection efficiency 96 hours after transfection. Immunofluorescent staining of β-tubulin was used to measure the length of RGCs′ axon. 4′, 6-diamidino-2-phenylindole staining was used to observe the nuclei of apoptotic cells. The mRNA level of Claudin-3 and VEGF was measured by real-time polymerase chain reaction. The protein levels of Claudin-3, vascular endothelial growth factor (VEGF), Bcl-2 and Caspase-3 was determined by Western blot. Results The positive transfection rate was more than 50% in both AAV-shScramble group and AAV-shClaudin-3 group. The length of RGCs' axon in AAV-shClaudin-3 group was shorter than that in normal control group and AAV-shScramble group (F=22 363.274,P＜0.05). Down-regulation of Claudin-3 accelerated RGCs' apoptosis with nuclei shrinkage, tapering, and nucleolus formation of apoptotic bodies. The mRNA levels of Claudin-3 and VEGF in AAV-shClaudin-3 group were lower than those in normal control group and AAV-shScramble group (F=257.408, 160.533;P＜0.05). The protein levels of Claudin-3, VEGF and Bcl-2 in AAV-shClaudin-3 group were lower than those in normal control group and AAV-shScramble group (F=129.671, 420.552, 62.669;P＜0.05), while the protein level of Caspase-3 in AAV-shClaudin-3 group was higher than that in normal control group and AAV-shScramble group (F=231.348,P＜0.05). Conclusion Down-regulation of Claudin-3 increases the expression of Caspase-3, reduces the expression of VEGF and Bcl-2, accelerates RGCs' apoptosis and inhibit the RGCs' axon growth.