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The Long Noncoding RNA CCAT2 Induces Chromosomal Instability Through BOP1-AURKB Signaling.

Baoqing Chen1, Mihnea P Dragomir2, Linda Fabris3

  • 1Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas; Department of Radiation Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China; Department of Thoracic Oncology, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Gastroenterology
|August 18, 2020
PubMed
Summary

High expression of colon cancer-associated transcript 2 (CCAT2) long noncoding RNA promotes chromosomal instability (CIN) and colorectal cancer progression by stabilizing the BOP1 protein. Targeting this CCAT2-BOP1 pathway may offer new treatments for microsatellite stable colorectal tumors.

Keywords:
AneuploidyMSSNoncoding RNATumorigenesis

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Chromosomal instability (CIN) is a hallmark of cancer, driving metastasis and therapeutic resistance through poorly understood mechanisms.
  • The long noncoding RNA (lncRNA) CCAT2 is linked to CIN in colon cancer, but its regulatory role remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which CCAT2 lncRNA contributes to chromosomal instability and colorectal cancer (CRC) pathogenesis.
  • To identify downstream targets of CCAT2 and their role in CIN.

Main Methods:

  • Cytogenetic analysis of CRC cell lines and CCAT2-transgenic mouse models.
  • Gene expression profiling and mass spectrometry to identify CCAT2 targets.
  • Protein interaction studies (MS2 pull-down, RNA immunoprecipitation) to characterize CCAT2-protein binding.
  • Functional assays assessing CIN, cell proliferation, and invasiveness upon target gene manipulation.
  • Analysis of patient cohorts to correlate CCAT2 and target gene expression with clinical outcomes.

Main Results:

  • CCAT2 overexpression induced CIN and chemoresistance in CRC cells and mouse models.
  • CCAT2 directly interacted with and stabilized the ribosomal biogenesis factor BOP1, increasing MYC-driven BOP1 expression.
  • BOP1 overexpression led to chromosomal missegregation, increased invasiveness, and promoted CIN by activating aurora kinase B.
  • Elevated CCAT2 and BOP1 levels correlated with microsatellite stable tumors and poorer patient survival.

Conclusions:

  • CCAT2 promotes CIN and carcinogenesis in colon cells by stabilizing BOP1, an aurora kinase B activator.
  • Targeting the CCAT2-BOP1 pathway presents a potential therapeutic strategy for microsatellite stable colorectal tumors.