RBM10 inhibits cell proliferation of lung adenocarcinoma via RAP1/AKT/CREB signalling pathway

Xin Jin1,2, Xin Di1, Ruimin Wang3

  • 1Department of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, Jilin, China.

Insights

RNA-binding motif protein 10 (RBM10) suppresses lung adenocarcinoma cell proliferation by inhibiting the RAP1/AKT/CREB pathway. RBM10 knockdown enhances proliferation, revealing its complex role in cancer.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • RNA-binding motif protein 10 (RBM10) has conflicting roles in cancer, with some studies suggesting tumor promotion.
  • Understanding RBM10's precise function in lung adenocarcinoma is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the role of RBM10 in lung adenocarcinoma cell proliferation.
  • To elucidate the molecular mechanisms underlying RBM10's effects on cancer growth.

Main Methods:

  • In vitro and in vivo experiments assessing cell proliferation with RBM10 overexpression and knockdown.
  • Complementary DNA microarray analysis to identify affected pathways.
  • Western blotting and pathway activators/inhibitors (EPAC, AKT pathway) to confirm molecular interactions.

Main Results:

  • RBM10 overexpression suppressed lung adenocarcinoma cell proliferation, while RBM10 knockdown enhanced it.
  • RBM10 was found to decrease RAP1 activation and CREB phosphorylation.
  • The proliferation effects were mediated through the RAP1/AKT/CREB signaling pathway, independent of MAPK/ERK and P38/MAPK.

Conclusions:

  • RBM10 acts as a suppressor of lung adenocarcinoma cell proliferation.
  • The RAP1/AKT/CREB pathway is a key mediator of RBM10's anti-proliferative effects in this cancer type.

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