Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05
  • 2024-06
  • 2024-07
  • A previous study showed that miR c

    2024-07-09

    A previous study showed that miR-200c is involved in glucose-mediated pathological processes (Zhang, Guan, & Jin, 2017). Glucose metabolism is critical for the growth and proliferation of both normal Ciclopirox ethanolamine australia and cancer cells, and reprogramming glucose metabolism now has been considered as a target of the treatment of malignancies (Hay, 2016). In this study, overexpression of miR-200c significantly reduced glucose uptake of cells of both human oral squamous cell carcinoma cell lines. In addition, miR-200c overexpression also significantly inhibited the proliferation of cancer cells. Those data indicate that overexpression of miR-200c may serve as a potential target for the treatment of oral squamous cell carcinoma. Activation of Akt signaling is common in nearly all of the human malignancies (Altomare & Testa, 2005). It has been reported that microRNA-200c targets Akt signaling pathway to inhibit cell apoptosis of pituitary adenoma (Liao et al., 2014). In addition, Akt signaling pathway regulates the expression of Glut-1, which plays a key role in glucose metabolism (Lo et al., 2011). In this study, microRNA-200c overexpression significantly upregulated the expression level of Glut-1 and phosphorylation level of Akt in oral squamous cell carcinoma cells. However, Akt activator treatment and Glut-1 overexpression showed no significant effect on miR-200c. Besides that, treatment with Akt activator SC79 for 1 hour significantly increased the expression level of Glut-1 in both oral squamous cell carcinoma cell lines, but Glut-1 overexpression showed no significant effects on levels of Akt and p-Akt. Those data suggest that miR-200c is an upstream inhibitor of Akt pathway, which is an upstream of Glut-1 in the pathogenesis of oral squamous cell carcinoma.
    Conclusion