RRS1 silencing suppresses colorectal cancer cell proliferation and tumorigenesis by inhibiting G2/M progression and

Xin-Lin Wu1, Zhi-Wen Yang1, Li He1

  • 1Department of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.

Oncotarget
|November 16, 2017
PubMed

Insights

Ribosome biogenesis regulatory protein homolog (RRS1) is overexpressed in colorectal cancer (CRC), promoting tumor growth and poor survival. Targeting RRS1 may offer a new therapeutic strategy for CRC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) is a leading global malignancy.
  • The role of Ribosome biogenesis regulatory protein homolog (RRS1) in CRC is not well understood.
  • RRS1 is crucial for ribosome biogenesis.

Purpose of the Study:

  • To investigate the role of RRS1 in colorectal cancer development and progression.
  • To explore RRS1 as a potential therapeutic target for CRC.

Main Methods:

  • Analysis of RRS1 expression in CRC tissues and correlation with patient survival.
  • In vitro studies involving RRS1 knockdown in CRC cell lines (RKO, HCT-116) to assess effects on cell cycle, apoptosis, proliferation, and angiogenesis.
  • In vivo tumor formation assays in nude mice.
  • Molecular analysis of key cell cycle regulators (CDC25C, CDK1, KI67, CDKN1A, p53).

Main Results:

  • RRS1 expression is significantly elevated in CRC tissues and linked to poorer patient survival.
  • RRS1 knockdown induced G2/M cell cycle arrest, apoptosis, and suppressed proliferation and angiogenesis in CRC cells.
  • RRS1 suppression reduced tumor formation in vivo.
  • Silencing RRS1 altered the expression of cell cycle regulators, including decreased CDC25C, CDK1, KI67 and increased CDKN1A, p53.

Conclusions:

  • RRS1 promotes colorectal cancer development and progression.
  • RRS1 is a potential prognostic biomarker and therapeutic target for CRC.

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