Aim: Emerging evidence has showed that long non-coding RNA (lncRNA) play an important role in the occurrence and development of various cancers. In the present study, the expression level of lincRNA-p21 was investigated in hepatocellular carcinoma (HCC), and its role in invasion of HCC was also explored.
Methods: The lincRNA-p21 levels in human HCC tumor tissue and cell lines HepG2 and SMMC-7721 were determined by real-time polymerase chain reaction. Transfected HCC cells with pcDNA-lincRNA-p21 or si-lincRNA-p21 for overexpression or downregulation of lincRNA-p21, the Notch signaling and epithelial-mesenchymal transition (EMT)-related proteins and cell invasion were measured by western blot and Transwell assay, respectively. A tumor xenotransplant mouse model was also established to investigate the role of lincRNA-p21 in tumor metastasis in vivo.
Results: The lincRNA-p21 expression was downregulated in HCC tissue and cells. Overexpression of lincRNA-p21 inhibited Notch singling and EMT, while its downregulation led to the reverse result. The invasion of HCC cell was also inhibited by pcDNA-lincRNA-p21, and activation of Notch signaling reversed this effect. In vivo, overexpression of lincRNA-p21 decreased the tumor metastasis, as well.
Conclusion: lincRNA-p21 was downregulated in HCC and lincRNA-p21 overexpression contributed to the inhibition of tumor invasion through mediating Notch signaling induced EMT.
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http://dx.doi.org/10.1111/hepr.12659 | DOI Listing |
Dev Biol
January 2025
Biology Department, Texas A&M University, College Station, TX 7843-3258. Electronic address:
During development of the vertebrate inner ear, sensory epithelia and neurons of the statoacoustic ganglion (SAG) arise from lineage-restricted progenitors that proliferate extensively before differentiating into mature post-mitotic cell types. Development of progenitors is regulated by Fgf, Wnt and Notch signaling, but how these pathways are coordinated to achieve an optimal balance of proliferation and differentiation is not well understood. Here we investigate the role in zebrafish of Foxm1, a transcription factor commonly associated with proliferation in developing tissues and tumors.
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Center for Pancreatic Cancer Research, The South China University of Technology School of Medicine, Guangzhou, Guangdong, China.
Pancreatic cancer is a highly lethal malignancy with few effective treatment options. Connexin 31 (Cx31) is a membrane protein capable of forming hexameric channels to facilitate the exchange of metabolites and signaling molecules. Yet, the contribution of Cx31 to the onset and progression of pancreatic cancer remains to be understood.
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January 2025
Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University.
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January 2025
Division of Oral and Systemic Health Sciences, School of Dentistry, University of California, Los Angeles, CA, 90095, USA; Department of Bioengineering, University of California, Los Angeles, CA, 90095, USA. Electronic address:
Exosomes derived from mesenchymal stem cells (MSCs) offer a promising alternative to traditional cell-based therapies for tissue repair by mitigating risks associated with the transplantation of living cells. However, insufficient osteogenic capacity of exosomes diminishes their potential in bone tissue regeneration. Here, we report novel osteogenically induced exosome mimetics (EMs) integrated into injectable hydrogel carriers for improved bone regeneration.
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Department of Conservative Dentistry & Endodontics, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 600077, Tamil Nadu, India. Electronic address:
Oral squamous cell carcinoma (OSCC) remains a major cause of morbidity and mortality worldwide with high recurrence rates and resistance to conventional therapies. Recent studies have highlighted the pivotal role of oral cancer stem cells (OCSCs) in driving treatment resistance and tumor recurrence. OCSCs possess unique properties, including self-renewal, differentiation potential, and resistance to chemotherapy and radiotherapy, which contribute to their ability to survive treatment and initiate tumor relapse.
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