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Published on: August 12, 2015
SP1 induced long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma proliferation via silencing of CDKN1A
Hao Ji1,2, Juan Wang1,2, Binbin Lu1,2
1Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Background:
LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration.
Methods:
We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1.
Results:
AGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA.
Conclusions:
We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.
Insights
The long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma (CCA) proliferation. Its upregulation in CCA tissues suggests AGAP2-AS1 is a potential therapeutic target for this cancer.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Long non-coding RNAs (LncRNAs) regulate gene expression through various mechanisms.
- The specific roles of LncRNAs in cholangiocarcinoma (CCA) pathogenesis remain largely unknown.
- Understanding LncRNA function in CCA is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression and function of the LncRNA AGAP2-AS1 in cholangiocarcinoma.
- To elucidate the molecular mechanisms underlying AGAP2-AS1's role in CCA progression.
Main Methods:
- Analysis of AGAP2-AS1 expression in 32 CCA tissues and two CCA cell lines.
- In vitro experiments involving AGAP2-AS1 knockdown and overexpression.
- Chromatin immunoprecipitation (CHIP) and RNA immunoprecipitation (RIP) assays to identify AGAP2-AS1 targets.
Main Results:
- AGAP2-AS1 was significantly upregulated in CCA tumor tissues compared to normal tissues.
- SP1 was identified as an inducer of AGAP2-AS1 expression in CCA.
- Knockdown of AGAP2-AS1 inhibited CCA cell proliferation and induced apoptosis.
- Overexpression of AGAP2-AS1 promoted CCA cell proliferation.
Conclusions:
- The LncRNA AGAP2-AS1 is upregulated in cholangiocarcinoma and promotes tumor cell proliferation.
- AGAP2-AS1 plays a significant role in CCA tumorigenesis.
- Targeting AGAP2-AS1 may represent a novel therapeutic strategy for cholangiocarcinoma.
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