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  • Open Access

    REVIEW

    An overview of autophagy in the differentiation of dental stem cells

    XITONG ZHAO, TIANJUAN JU, XINWEI LI, CHANGFENG LIU, LULU WANG*, LI-AN WU*

    BIOCELL, Vol.48, No.1, pp. 47-64, 2024, DOI:10.32604/biocell.2023.045591 - 30 January 2024

    Abstract Dental stem cells (DSCs) have attracted significant interest as autologous stem cells since they are easily accessible and give a minimal immune response. These properties and their ability to both maintain self-renewal and undergo multi-lineage differentiation establish them as key players in regenerative medicine. While many regulatory factors determine the differentiation trajectory of DSCs, prior research has predominantly been based on genetic, epigenetic, and molecular aspects. Recent evidence suggests that DSC differentiation can also be influenced by autophagy, a highly conserved cellular process responsible for maintaining cellular and tissue homeostasis under various stress conditions. This… More >

  • Open Access

    ARTICLE

    LncRNA CACNA1G-AS1 up-regulates FTH1 to inhibit ferroptosis and promote malignant phenotypes in ovarian cancer cells

    YANPING JIN1, JIANPING QIU1, XIUFANG LU1, YAN MA1, GUOWEI LI2,*

    Oncology Research, Vol.31, No.2, pp. 169-179, 2023, DOI:10.32604/or.2023.027815 - 10 April 2023

    Abstract Previous study revealed that ferritin heavy chain-1 (FTH1) could regulate ferritinophagy and affect intracellular Fe2+ content in various tumors, while its N6-methyladenosine (m6A) RNA methylation was closely related the prognosis of ovarian cancer patients. However, little is known about the role of FTH1 m6A methylation in ovarian cancer (OC) and its possible action mechanisms. In this study we constructed FTH1 m6A methylation regulatory pathway (LncRNA CACNA1G-AS1/IGF2BP1) according to related bioinformatics analysis and research, through clinical sample detections we found that these pathway regulatory factors were significantly up-regulated in ovarian cancer tissues, and their expression levels were More >

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