Abnormal expression of p63 has been well identified in multiple malignancies. However, little study has been done on the association between p63 and chondro sarcoma. In the current study, we mainly explored the expression of p63 in different grades of chondrosarcoma. Our data showed that p63 was significantly decreased in grade II and III chondrosarcoma compared with that of grade I chondrosarcoma and normal control. As the characteristic of grade II and III chondrosarcoma is metastasis, we then searched the function of p63 chondrosarcoma. In vitro study showed that overexpression of p63 significantly suppressed chondrosarcoma cell viability, migration and invasion. Meanwhile, upregualtion of p63 induced chondrosarcoma cell apoptosis. Furthermore, we showed that overexpression of p63 could significantly increase the protein expression of PTEN. In contrast, silencing of PTEN markedly reduced the protein levels of Bax, and enhanced the expression of PCNA and p27, even in cells transfected with p-p63. These data showed that p63 was a tumor suppressor mainly through regulating PTEN in chondrosarcoma cells. In summary, reduction of p63 in grade II and III chondrosarcoma enhances the malignant phenotype mainly through modulating the expression of PTEN.
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http://dx.doi.org/10.1691/ph.2017.6400 | DOI Listing |
Int J Mol Sci
December 2024
Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City 32897, Egypt.
Cancer cells undergo metabolic rewiring to support rapid proliferation and survival in challenging environments. Glutamine is a preferred resource for cancer metabolism, as it provides both carbon and nitrogen for cellular biogenesis. Recent studies suggest the potential anticancer activity of amino acid analogs.
View Article and Find Full Text PDFBrain Res
January 2025
Department of Traditional Chinese Medicine Pharmacy, Wenling Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University, Taizhou 317500, China. Electronic address:
Background: Neuronal survival and regeneration are critical aspects of recovery from ischemic brain injuries. Astragaloside IV (AS-IV), a saponin extracted from the traditional Chinese medicine Astragalus membranaceus, has shown promise in promoting neuronal health. This study investigates the effects of AS-IV on neuronal survival and apoptosis post-oxygen-glucose deprivation (OGD), focusing on the modulation of the PTEN/AKT signaling pathway.
View Article and Find Full Text PDFMedicine (Baltimore)
January 2025
Opthalmology, Chongqing Hechuan District People's Hospital, Chongqing, China.
Background: Bushen-Huoxue-Mingmu-Formula (MMF) has achieved definite clinical efficacy. However, its mechanism is still unclear.
Objective: Investigating the molecular mechanism of MMF to protect retinal ganglion cells (RGCs).
Breast Cancer Res Treat
January 2025
Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, 6205, Bangladesh.
Background: Globally, Breast Cancer (BC) is the most frequent cancer in women and has a major negative impact on the physical and emotional well-being of its patients as well as one of the most common cancers to be diagnosed. Numerous studies have been published to identify various molecular pathways, including PI3K/AKT/PTEN. Moreover, growing evidence suggests that miRNAs have been found to play a vital role in the growth and carcinogenesis of tumors.
View Article and Find Full Text PDFFASEB J
January 2025
State Key Laboratory of Virology, Institute of Medical Virology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan, Hubei, China.
Hantaan virus (HTNV) infection causes severe hemorrhagic fever with renal syndrome (HFRS) in humans and the infectious process can be regulated by autophagy. The phosphatase and tensin homolog (PTEN) protein has antiviral effects and plays a critical role in the autophagy pathway. However, the relationship between PTEN and HTNV infection is not clear and whether PTEN-regulated autophagy involves in HTNV replication is unknown.
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