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NOD1 inhibits proliferation and enhances response to chemotherapy via suppressing SRC-MAPK pathway in hepatocellular

Xiaomin Ma1, Yumin Qiu1, Lihui Zhu1

  • 1Shandong Provincial Key Laboratory of Infection & Immunology, Department of Immunology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, 250012, China.

Journal of Molecular Medicine (Berlin, Germany)
|December 25, 2019
PubMed

Insights

NOD1, an innate immune sensor, suppresses liver cancer (HCC) growth by inhibiting the SRC/MAPK pathway. Overexpressing NOD1 also enhances HCC cell sensitivity to chemotherapy, offering new therapeutic strategies.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is an innate immune sensor with a known role in infection.
  • The function of NOD1 in cancer, particularly hepatocellular carcinoma (HCC), remains largely uninvestigated.

Purpose of the Study:

  • To investigate the role of NOD1 in hepatocellular carcinoma progression and its potential as a therapeutic target.

Main Methods:

  • Analysis of NOD1 expression in HCC tissues.
  • In vivo and in vitro experiments assessing the effects of NOD1 overexpression on HCC cell proliferation and tumorigenesis.
  • Investigation of the molecular mechanisms involving SRC and the SRC/MAPK pathway.
  • Evaluation of NOD1's impact on HCC cell response to chemotherapy (sorafenib, 5-FU).

Main Results:

  • NOD1 expression was significantly decreased in HCC tissues.
  • NOD1 overexpression inhibited HCC tumorigenesis in vivo and HCC cell proliferation in vitro by inducing G1 phase cell cycle arrest.
  • NOD1 directly targeted proto-oncogene SRC, inhibiting SRC activation and suppressing the SRC/MAPK axis.
  • NOD1 enhanced the efficacy of sorafenib and 5-FU chemotherapy in HCC cells both in vitro and in vivo.

Conclusions:

  • NOD1 acts as a tumor suppressor in hepatocellular carcinoma.
  • NOD1 inhibits HCC proliferation and tumorigenesis by targeting the SRC/MAPK signaling pathway.
  • NOD1 enhances chemosensitivity in HCC, suggesting its potential as a therapeutic agent or target.
Keywords:
ChemosensitivityHepatocellular carcinomaMAPKNOD1SRC

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