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UCA1, a long noncoding RNA, promotes the proliferation of CRC cells via p53/p21 signaling

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AbstractObjectiveRecently, the role of long noncoding RNAs (lncRNAs) in human colorectal cancer (CRC) has been a subject of intense focus. We set out to determine the function of one lncRNA, termed urothelial carcinoma-associated 1 (UCA1) in CRC cell proliferation and its underlying mechanisms.MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expression level of UCA1 in 50 pairs of CRC samples compared with non-tumor colon tissues. Cell growth was determined using the Cell Counting Kit-8 (CCK-8). Western blotting was carried out to analyze the related protein expression. Flow cytometry was done to evaluate cell apoptosis by UCA1 inhibition.ResultsWe found an increased expression of UCA1 in CRC samples. Knockdown of UCA1 in HCT116 cells induced a decrease in cell proliferation rate compared to control samples. This oncogenic activity may be enhanced through p53/ p21 signaling.ConclusionOur results supported the hypothesis that upregulation of UCA1 contributes to the unlimited proliferation rate of CRC cells, at least partially through the negative regulation of p53/p21 signaling pathway. Finally, we found that UCA1 merely influenced CRC cell apoptosis.
Title: UCA1, a long noncoding RNA, promotes the proliferation of CRC cells via p53/p21 signaling
Description:
AbstractObjectiveRecently, the role of long noncoding RNAs (lncRNAs) in human colorectal cancer (CRC) has been a subject of intense focus.
We set out to determine the function of one lncRNA, termed urothelial carcinoma-associated 1 (UCA1) in CRC cell proliferation and its underlying mechanisms.
MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expression level of UCA1 in 50 pairs of CRC samples compared with non-tumor colon tissues.
Cell growth was determined using the Cell Counting Kit-8 (CCK-8).
Western blotting was carried out to analyze the related protein expression.
Flow cytometry was done to evaluate cell apoptosis by UCA1 inhibition.
ResultsWe found an increased expression of UCA1 in CRC samples.
Knockdown of UCA1 in HCT116 cells induced a decrease in cell proliferation rate compared to control samples.
This oncogenic activity may be enhanced through p53/ p21 signaling.
ConclusionOur results supported the hypothesis that upregulation of UCA1 contributes to the unlimited proliferation rate of CRC cells, at least partially through the negative regulation of p53/p21 signaling pathway.
Finally, we found that UCA1 merely influenced CRC cell apoptosis.

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