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Mitochondrial NOS1 suppresses apoptosis in colon cancer cells through increasing SIRT3 activity

Qianli Wang1, Shuangyan Ye2, Xi Chen2

  • 1Cancer Research Institute, Southern Medical University, Guangzhou, 510515, China; Guangdong Provincial Key Laboratory of Cancer Immunotherapy Research, Guangzhou, 510515, China; Guangzhou Key Laboratory of Tumor Immunology Research, Southern Medical University, Guangzhou, 510515, China.

Biochemical and Biophysical Research Communications
|June 3, 2019
PubMed

Insights

Nitric oxide synthase 1 (NOS1) in colon cancer cells inhibits apoptosis by translocating to mitochondria. This mitochondrial NOS1 enhances SIRT3 activity, reducing superoxide levels and conferring resistance to chemotherapy, a process reversible by blocking NOS1 mitochondrial entry.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Signaling

Background:

  • Nitric oxide (NO) synthesis by nitric oxide synthase (NOS) is implicated in colon cancer, but the specific role of NOS1 remains unclear.
  • Existing research has primarily focused on NOS2 and NOS3, neglecting the potential contribution of NOS1 in colon cancer progression.

Purpose of the Study:

  • To investigate the specific role of nitric oxide synthase 1 (NOS1) in colon cancer.
  • To elucidate the mechanism by which NOS1 influences colon cancer cell behavior, particularly apoptosis and chemoresistance.

Main Methods:

  • Construction of colon cancer cells with stable overexpression of NOS1.
  • Observation of NOS1 protein localization within mitochondria.
  • Assessment of mitochondrial superoxide levels and apoptosis induction (e.g., using cisplatin).
  • Investigation of the effect of Geldanamycin (Hsp90 inhibitor) on NOS1 translocation and apoptosis resistance.
  • Evaluation of SIRT3 activity and its relationship with NOS1 and mitochondrial superoxide.

Main Results:

  • NOS1 protein was localized in the mitochondria of colon cancer cells.
  • NOS1 inhibited both basal and cisplatin-induced mitochondrial superoxide production and reduced cisplatin-induced apoptosis.
  • Inhibiting NOS1 mitochondrial translocation with Geldanamycin reversed NOS1-mediated apoptosis resistance.
  • NOS1 enhanced SIRT3 activity, contributing to lower mitochondrial superoxide and apoptosis resistance via the mtNOS1-SIRT3-SOD2 axis.

Conclusions:

  • NOS1 plays a significant role in promoting apoptosis resistance in colon cancer cells.
  • The mechanism involves NOS1 translocation to mitochondria, enhancing SIRT3 activity, and subsequently reducing mitochondrial superoxide.
  • Targeting NOS1 mitochondrial translocation presents a potential therapeutic strategy to overcome chemoresistance in colon cancer.
Keywords:
ApoptosisColon cancerMitochondriaNitric oxide synthase 1SIRT3

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