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Biological effects of NODAL on endometrial cancer cells and its underlying mechanisms

Xiaoshan Hong1, Bin Wen1, Huaming Zhang1

  • 1Department of Gynecology, Guangdong Women and Children Hospital, Guangzhou, Guangdong 510010, P.R. China.

Experimental and Therapeutic Medicine
|March 15, 2021
PubMed

Insights

Nodal growth differentiation factor (NODAL) and activin A receptor type 1C (ALK7) are decreased in endometrial cancer. NODAL inhibits cancer progression and promotes apoptosis by activating ALK7, suggesting a therapeutic target for endometrial cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Activin A receptor type 1C (ALK7) and its ligand, nodal growth differentiation factor (NODAL), are implicated in cancer cell functions like invasion, migration, and apoptosis.
  • While NODAL promotes breast cancer cell apoptosis via ALK7 activation, their specific roles and mechanisms in endometrial cancer (EC) remain unclear.

Purpose of the Study:

  • To investigate the expression of NODAL and ALK7 in endometrial cancer (EC) cells.
  • To elucidate the underlying mechanisms of NODAL and ALK7 in regulating EC cell proliferation, invasion, migration, and apoptosis.

Main Methods:

  • Quantitative PCR and western blotting were used to assess ALK7 and NODAL expression levels.
  • Cell proliferation, invasion, and migration were evaluated using Cell Counting Kit-8, Transwell, and wound healing assays, respectively.
  • Apoptosis and related protein expression were analyzed via flow cytometry and western blotting following NODAL overexpression or ALK7 interference.

Main Results:

  • NODAL and ALK7 expression levels were significantly lower in EC cell lines compared to normal endometrial cells.
  • NODAL overexpression suppressed EC cell proliferation, invasion, and migration, while enhancing apoptosis.
  • NODAL overexpression led to increased ALK7 expression, and ALK7 interference reversed the inhibitory effects of NODAL on EC cells.

Conclusions:

  • NODAL inhibits endometrial cancer cell proliferation, invasion, and migration.
  • NODAL exerts its tumor-suppressive effects in EC by activating ALK7.
  • The NODAL-ALK7 pathway represents a potential therapeutic target for endometrial cancer treatment.
Keywords:
activin A receptor type 1Capoptosisendometrial cancerinvasionmigrationnodal growth differentiation factor

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