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RSL1D1 promotes the progression of colorectal cancer through RAN-mediated autophagy suppression

Xunhua Liu1,2, Jianxiong Chen1,2, Xiaoli Long1,2

  • 1Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

Cell Death & Disease
|January 11, 2022
PubMed

Insights

Ribosomal L1 domain containing 1 (RSL1D1) is elevated in colorectal cancer (CRC) and promotes tumor growth by inhibiting autophagy. Targeting the RSL1D1/RAN/STAT3 pathway may offer new CRC treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Ribosomal protein RSL1D1 is a potential colorectal cancer (CRC) target, but its function in cancer is unclear.
  • Understanding RSL1D1's role is crucial for developing novel CRC therapies.

Purpose of the Study:

  • To investigate the role of RSL1D1 in colorectal cancer progression.
  • To elucidate the molecular mechanisms underlying RSL1D1's function in CRC.
  • To evaluate RSL1D1 as a potential therapeutic target for CRC.

Main Methods:

  • Quantitative analysis of RSL1D1 expression in CRC tumors and patient data.
  • Functional assays to assess the impact of RSL1D1 on CRC cell proliferation, invasion, and metastasis.
  • Investigation of RSL1D1's interaction with RAN and its effect on RAN deacetylation by Sirt7.
  • Analysis of RSL1D1's influence on nuclear STAT3 accumulation and STAT3-regulated autophagy.

Main Results:

  • RSL1D1 expression is significantly upregulated in CRC tumors.
  • High RSL1D1 expression correlates with poorer patient survival.
  • RSL1D1 promotes CRC cell proliferation, invasion, and metastasis by suppressing autophagy.
  • RSL1D1 interacts with RAN, inhibiting its deacetylation by Sirt7, which affects nuclear STAT3 accumulation and autophagy.

Conclusions:

  • The RSL1D1/RAN/STAT3 regulatory axis plays a critical role in CRC autophagy and tumor progression.
  • RSL1D1 is a promising therapeutic target for colorectal cancer treatment.

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