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Super-enhancer-associated long noncoding RNA RP11-569A11.1 inhibited cell progression and metastasis by regulating

Huanhuan Chen1, Junyu Zheng1, Linping Yan1

  • 1Department of Clinical Laboratory, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital and Jiangsu Institute of Cancer Research, Nanjing, China.

Journal of Clinical Laboratory Analysis
|May 4, 2021
PubMed
Abstract

Insights

Super-enhancer-associated long noncoding RNAs (SE-LncRNAs) are key in cancer. This study identified RP11-569A11.1 as a novel SE-LncRNA that inhibits colorectal cancer (CRC) progression by regulating IFIT2, suggesting its potential as a diagnostic biomarker.

Area of Science:

  • Molecular oncology
  • Cancer genomics
  • Long noncoding RNA research

Background:

  • Super-enhancer-associated long noncoding RNAs (SE-LncRNAs) play critical roles in carcinogenesis.
  • This study focuses on identifying and characterizing a novel SE-LncRNA, RP11-569A11.1, in the context of colorectal cancer (CRC) progression.

Purpose of the Study:

  • To identify novel super-enhancer-associated long noncoding RNAs (SE-LncRNAs) involved in colorectal cancer (CRC).
  • To investigate the functional role of the identified SE-LncRNA, RP11-569A11.1, in CRC progression.
  • To evaluate RP11-569A11.1 as a potential diagnostic biomarker for CRC.

Main Methods:

  • SE-LncRNA microarray and RT-qPCR were used to identify and quantify differentially expressed SE-LncRNAs in CRC tissues and cells.
  • Functional assays (CCK-8, colony formation, flow cytometry, Transwell) assessed the impact of RP11-569A11.1 on CRC cell behavior.
  • RNA-sequencing and Western blot analyses elucidated the molecular mechanism, focusing on the regulation of interferon-induced protein with tetratricopeptide repeat 2 (IFIT2).

Main Results:

  • A total of 23 significantly expressed SE-LncRNAs were identified in CRC, with RP11-569A11.1 being notably downregulated.
  • RP11-569A11.1 demonstrated diagnostic potential with an AUC of 0.77, indicating good sensitivity (74.29%) and specificity (71.43%).
  • Overexpression of RP11-569A11.1 suppressed CRC cell proliferation, migration, and invasion while inducing apoptosis, with knockdown yielding opposite effects. RP11-569A11.1 positively regulated IFIT2 expression.

Conclusions:

  • RP11-569A11.1 inhibits colorectal cancer (CRC) tumorigenesis through an IFIT2-dependent mechanism.
  • RP11-569A11.1 shows promise as a diagnostic biomarker for CRC.
Keywords:
IFIT2RP11-569A11.1colorectal cancerdiagnostic biomarkersuper-enhancer-associated long noncoding RNA

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