Browsing by Subject "PI3K/AKT pathway"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Open Access
    Downregulation of PDCD10 mitigates the malignant biological behavior and increases the sensitivity of esophageal squamous cell carcinoma cells to radiotherapy by inhibiting the PI3K/AKT pathway
    (2026) Qisong Chen; Qing Gao; Junkai Xu; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologia
    The intensification of radiotherapy is an effective way to improve the therapeutic efficacy of radiation-sensitive malignancies such as esophageal cancer (EC). Esophageal squamous cell carcinoma (ESCC) accounts for 85% of all EC cases worldwide, with a relatively higher incidence and mortality in East Asia. In this study, we explored the functions and mechanisms of programmed cell death 10 (PDCD10) in the malignancy and radiotherapy sensitivity of ESCC cells. We observed that PDCD10 is highly expressed in ESCC tissues and is correlated with a poor prognosis in patients with ESCC. PDCD10 downregulation suppressed ESCC cell proliferation, migration, and invasion but promoted apoptosis. In addition, it enhanced ionizing radiation (IR)-induced ESCC cell damage, whereas PDCD10 overexpression had the opposite effect. Mechanistically, PDCD10 increased the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in ESCC cell lines. The administration of LY294002, a PI3K inhibitor, significantly inhibited the oncogenic functions of PDCD10, leading to an increase in IR-induced cell damage. These findings establish PDCD10 as a critical intrinsic regulator of the sensitivity of ESCC cells to IR through the modulation of the PI3K/AKT pathway.
  • Thumbnail Image
    Publication
    Open Access
    The CCL27-CCR10 axis contributes to promoting proliferation, migration, and invasion of lung squamous cell carcinoma
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Li, Baijun; Wei, Caizhou; Zhong, Yonglong; Huang, Jianwei; Li, Rizhu
    Lung cancer is characterized by its high mortality and morbidity. A deep understanding of the molecular mechanisms of lung cancer tumorigenesis helps to develop novel lung cancer diagnostic and therapeutic strategies. However, the picture of the associated molecular landscape is not yet complete. As understood, chemokine-receptor interactions contribute much to lung cancer tumorigenesis, in which CCR10 also plays an important role. This study aimed to expand the knowledge of CCR10 in lung squamous cell carcinoma (LUSC) in the manner of molecular mechanism and biological functions. Using GEPIA database, the survival analysis between LUSC patients with high and low CCR10 expressions was performed, showing that CCR10 could be regarded as a risk factor for LUSC patients. Subsequently, CCR10 protein and mRNA expressions in LUSC were examined by qRTPCR and western blot respectively. The results indicated that CCR10 was highly expressed in LUSC cells. The results of CCK-8, colony formation, and Transwell assays presented that CCL27, the ligand of CCR10, promoted proliferative, migratory, and invasive abilities of LUSC cells by activating CCR10. Also, the PI3K/AKT signaling pathway was verified as the involved pathway by western blot. Overall, it could be concluded that the CCL27-CCR10 regulatory axis can activate the PI3K/AKT pathway fostering the malignant features of LUSC cells.