Background: This study aimed to investigate the effect of LAMA5 on palatal development in mice.
Methods: The palatine process of C57BL/6 J fetal mice on the embryonic day 13.5 (E13.5) was cultured in vitro via the rotating culture method. The LAMA5-shRNA adenovirus vector was constructed, then transfected into the palatal process of E13.5 for 48 h in vitro. A fluorescence microscope was used to visualize the fusion of palates. The expression of LAMA5 was also detected. The expression of ki67, cyclin D1, caspase 3, E-cadherin, vimentin and SHH signaling pathway-related signaling factors in the blank control group, the negative control group, and the LAMA5 interference group were detected after virus transfection.
Results: The bilateral palates in the LAMA5 interference group were not fused after virus transfection. PCR and WB showed that the mRNA and protein expressions of LAMA5 were decreased in the LAMA5 interference group. Furthermore, the mRNA and protein expressions of ki67, cyclin D1 and gli1 were decreased in the LAMA5 interference group, while the mRNA and protein expressions of caspase 3 were increased. However, the mRNA and protein expression of E-cadherin, vimentin, Shh and ptch1 did not significantly change in the LAMA5 interference group.
Conclusions: LAMA5 silencing causes cleft palate by inhibiting the proliferation of mouse palatal cells and promoting apoptosis, which may not be involved in EMT. LAMA5 silencing can also cause cleft palate by interfering with the SHH signaling pathway.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10957387 | PMC |
http://dx.doi.org/10.1016/j.bj.2023.100627 | DOI Listing |
Biomed J
April 2024
Department of Oral and Maxillofacial Surgery, the Affiliated Hospital of Qingdao University, Qingdao, Shandong, China; Department of Stomatology, Qingdao University, Qingdao, Shandong, China. Electronic address:
Background: This study aimed to investigate the effect of LAMA5 on palatal development in mice.
Methods: The palatine process of C57BL/6 J fetal mice on the embryonic day 13.5 (E13.
Onco Targets Ther
February 2021
Department of Clinical Laboratory, Hangzhou Cancer Hospital, Hangzhou, Zhejiang, 320000, People's Republic of China.
Introduction: Esophageal squamous cell carcinoma (ESCC) is often resistant to radiotherapy, likely due to sub-clones that survive and repopulate in the tumor. The analysis of genomic sequencing data related to radiotherapy will provide a better understanding of the intratumoral heterogeneity and genetic evolution of ESCC during radiotherapy.
Methods: We analyzed whole-exome sequencing data from pre- and post-irradiation ESCC patients at single-cell and bulk levels in public datasets.
Mutations in the Fms-related tyrosine kinase 4 (FLT4) and forkhead box protein C2 (FOXC2) genes cause Milroy disease (MD) and lymphedema-distichiasis syndrome (LDS), respectively, but the mechanism underlying disease pathology remains unclear. Applying whole-exome sequencing to two families with MD, one LDS family, and one sporadic LDS case, we identified four rare variants in the laminin subunit alpha-5 gene (LAMA5) in subjects carrying novel and known missense FLT4 mutations and a 7-bp duplication and 1-bp insertion in FOXC2. Phenotyping was expanded in some individuals using magnetic resonance lymphangiography, indiocyanine green fluorescence lymphography, and immunofluorescent lymphatic staining of skin tissue.
View Article and Find Full Text PDFMol Cancer Res
January 2014
Department of Biology, University of Iowa, Iowa City, IA, 52242 USA.
Unlabelled: Significant evidence implicates α3β1 integrin in promoting breast cancer tumorigenesis and metastasis-associated cell behaviors in vitro and in vivo. However, the extent to which α3β1 is actually required for breast cancer metastasis remains to be determined. We used RNA interference to silence α3 integrin expression by approximately 70% in 4T1 murine mammary carcinoma cells, a model of aggressive, metastatic breast cancer.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!