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AIM2 promotes non-small-cell lung cancer cell growth through inflammasome-dependent pathway

Minda Zhang1, Chenyu Jin1, Yunjia Yang1

  • 1State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing, China.

Journal of Cellular Physiology
|April 7, 2019
PubMed

Insights

The human absent in melanoma 2 (AIM2) gene promotes non-small-cell lung cancer (NSCLC) growth by activating the inflammasome pathway. Suppressing AIM2 halts cancer cell proliferation and tumor development in NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • The human absent in melanoma 2 (AIM2) is a DNA sensor with debated roles in cancer.
  • Previous research indicated AIM2 as a tumor suppressor, but recent findings suggest oncogenic functions in various cancers.
  • The specific role of AIM2 in non-small-cell lung cancer (NSCLC) remains largely undetermined.

Purpose of the Study:

  • To investigate the role of AIM2 in non-small-cell lung cancer (NSCLC).
  • To elucidate the underlying mechanism of AIM2's function in NSCLC progression.

Main Methods:

  • Quantitative analysis of AIM2 expression in NSCLC cells.
  • In vitro and in vivo assays to assess tumor-promoting properties.
  • AIM2 knockdown using short hairpin RNA (shRNA) and overexpression studies.
  • Assessment of cell cycle progression (G2/M phase).
  • Analysis of inflammasome formation and activation.
  • Inhibition of inflammasome pathway using caspase-1 inhibitor (VX-765) and ASC siRNA.

Main Results:

  • AIM2 is highly expressed in NSCLC cells, indicating a tumor-promoting role.
  • AIM2 suppression via shRNA led to cell proliferation arrest at the G2/M phase.
  • AIM2 modulated inflammasome formation; knockdown reduced it, while overexpression or poly(dA:dT) stimulation induced it.
  • Inflammasome blockade reversed the effects of AIM2 manipulation on cell proliferation.

Conclusions:

  • AIM2 functions as an oncogene in non-small-cell lung cancer (NSCLC).
  • AIM2 promotes NSCLC progression through an inflammasome-dependent mechanism.
  • Targeting AIM2 or the inflammasome pathway may offer therapeutic strategies for NSCLC.
Keywords:
AIM2cell cycleinflammasomenon-small-cell lung cancer

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