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RNF216 contributes to proliferation and migration of colorectal cancer via suppressing BECN1-dependent autophagy

Hui Wang1, Yanan Wang1, Liu Qian1

  • 1Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine (SJTUSM) and Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences & SJTUSM, Shanghai, China.

Oncotarget
|May 21, 2016
PubMed

Insights

Ring finger protein 216 (RNF216) promotes colorectal cancer (CRC) growth by degrading BECN1, a tumor suppressor, thus inhibiting autophagy. Targeting RNF216 may offer a new therapeutic strategy for CRC.

Area of Science:

  • Oncology
  • Cellular Biology
  • Molecular Mechanisms

Background:

  • Autophagy is crucial for cellular homeostasis; its dysfunction is linked to tumor formation.
  • Ring finger protein 216 (RNF216) is an E3 ligase involved in toll-like receptor (TLR) signaling and autophagy.
  • Dysregulated autophagy contributes to colorectal cancer (CRC) progression.

Purpose of the Study:

  • To investigate the role of RNF216 in colorectal cancer (CRC) development.
  • To elucidate the molecular mechanisms by which RNF216 influences CRC cell behavior.
  • To evaluate RNF216 as a potential therapeutic target for CRC.

Main Methods:

  • Analysis of RNF216 expression in human CRC tissues and cell lines.
  • In vitro and in vivo experiments assessing CRC cell proliferation and migration.
  • Investigation of RNF216's effect on BECN1 levels and autophagy.
  • RNA interference (knockdown) to study the functional consequences of RNF216 or BECN1 depletion.

Main Results:

  • RNF216 was upregulated in CRC tissues and cell lines, correlating with CRC progression.
  • RNF216 enhanced CRC cell proliferation and migration by promoting BECN1 proteasomal degradation.
  • RNF216 inhibited BECN1-dependent autophagy in CRC cells, particularly under starvation.
  • RNF216 knockdown increased autophagy, suppressing CRC cell proliferation and migration.

Conclusions:

  • RNF216 promotes CRC cell proliferation and migration by negatively regulating BECN1-dependent autophagy.
  • RNF216 acts as an oncoprotein in colorectal cancer.
  • RNF216 represents a potential biomarker and a novel therapeutic target for CRC treatment.
Keywords:
BECN1RNF216autophagycolorectal cancer

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