LMNB1 deletion in ovarian cancer inhibits the proliferation and metastasis of tumor cells through PI3K/Akt pathway
Experimental Cell Research, ISSN: 0014-4827, Vol: 426, Issue: 2, Page: 113573
2023
- 6Citations
- 7Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations6
- Citation Indexes6
- Captures7
- Readers7
Article Description
Ovarian cancer (OC) is a common malignant tumor in gynecology. LMNB1 is an important component of the nuclear skeleton. The expression of LMNB1 in ovarian cancer is significantly higher than that in normal tissues, but its role in tumor still needs comprehensive investigation. In this study, we overexpressed and knocked down LMNB1 in ovarian cancer cells and explore the effect of LMNB1 on the cell proliferation, migration and the underlying mechanism. We analyzed the expression levels of LMNB1 in ovarian cancer and their clinical relevance by using bioinformatics methods, qRT-PCR, Western blot and immunohistochemistry. To state the effect and mechanism of LMNB1 on OC in vitro and in vivo, we performed mouse xenograft studies, CCK8, cloning formation, Edu incorporation, wound healing, transwell and flow cytometry assay in stable LMNB1 knockdown OC cells, following by RNA-seq. Overexpression of LMNB1 indicates the progression of OC. LMNB1 knockdown inhibited the proliferation and migration of OC cells by suppressing the FGF1-mediated PI3K-Akt signaling pathway. Our study shows LMNB1 as a novel prognostic factor and therapeutic target in OC.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0014482723001209; http://dx.doi.org/10.1016/j.yexcr.2023.113573; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85151426274&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/37003558; https://linkinghub.elsevier.com/retrieve/pii/S0014482723001209; https://dx.doi.org/10.1016/j.yexcr.2023.113573
Elsevier BV
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