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Published on: March 30, 2019
Long Noncoding RNA ANRIL Regulates Proliferation of Non-small Cell Lung Cancer and Cervical Cancer Cells
Madoka Naemura1, Chihiro Murasaki1, Yasutoshi Inoue1
1Department of Biological and Environmental Chemistry, Faculty of Humanity-Oriented Science and Engineering, Kinki University, Fukuoka, Japan.
Background:
Long noncoding RNA ANRIL (antisense non-coding RNA in the INK4 locus) represses p15 and p16, which induce cell-cycle arrest at G1 phase, leading to enhanced cell proliferation of normal fibroblasts. Herein we report that ANRIL is also involved in the regulation of cancer-cell proliferation.
Materials And Methods:
HeLa and H1299 cells were transfected with ANRIL siRNAs. At 72 h post-transfection, cells were subjected to quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and cell-cycle analysis.
Results:
qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells.
Conclusion:
ANRIL positively regulates the proliferation of cancer cells, such as H1299 and HeLa cells, via regulating p15 and other genes related to G2/M phase control.
Insights
Long noncoding RNA ANRIL promotes cancer cell proliferation by inhibiting p15 expression. Depleting ANRIL halts cancer cell cycle progression at G2/M phase, inhibiting growth.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Long noncoding RNA ANRIL (antisense non-coding RNA in the INK4 locus) normally represses p15 and p16, promoting normal fibroblast proliferation.
- ANRIL's role in cancer cell proliferation was investigated.
Purpose of the Study:
- To determine the involvement of ANRIL in cancer cell proliferation.
- To elucidate the regulatory mechanisms of ANRIL in cancer cells.
Main Methods:
- HeLa and H1299 cancer cells were transfected with ANRIL siRNAs.
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and cell-cycle analysis were performed.
Main Results:
- ANRIL was highly expressed in cancer cells compared to normal fibroblasts.
- ANRIL depletion increased p15 expression and caused cell-cycle arrest at G2/M phase.
- Cancer cell proliferation was inhibited upon ANRIL depletion.
Conclusions:
- ANRIL positively regulates cancer cell proliferation (H1299, HeLa).
- ANRIL exerts its function by regulating p15 and other G2/M phase-related genes.
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