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LINC00052 functions as a tumor suppressor through negatively modulating miR-330-3p in pancreatic cancer
Xingcheng Xiong1, Qiao Shi1, Xiaojia Yang2
1Department of Pancreatic Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Abstract:
Pancreatic cancer is a serious solid malignant tumor worldwide. Increasing evidence has pointed out that abnormal expressions of long noncoding RNAs are involved in various tumors. Meanwhile, LINC00052 is reported as a famous tumor regulator in several cancers. Nevertheless, the biological role of LINC00052 in pancreatic cancer progression is still unknown. Our study was to explore the specific mechanism of LINC00052 in pancreatic cancer. First, we observed that the LINC00052 was obviously downregulated in several pancreatic cancer cell lines. Overexpression of LINC00052 greatly repressed AsPC-1 and SW1990 cell proliferation, triggered the apoptosis and prevented cell cycle in the G1 phase. For another, AsPC-1 and SW1990 cell migration and invasion capacity were also obviously repressed by LINC00052 upregulation. Moreover, miR-330-3p was elevated in pancreatic cancer cells and can function as a target of LINC00052 confirmed by luciferase reporter and RNA Immunoprecipitation (RIP) experiments. Inhibition of miR-330-3p could depress pancreatic cancer progression while overexpressed miR-330-3p exhibited an opposite process. Finally, our data indicated that the LINC00052 also remarkably suppressed pancreatic tumor growth via modulating miR-330-3p in vivo. To conclude, our study revealed that the LINC00052 might provide a new perspective for pancreatic cancer therapy.
Insights
Long noncoding RNA LINC00052 is downregulated in pancreatic cancer. Upregulating LINC00052 inhibits tumor cell proliferation, apoptosis, and migration, offering a potential new therapy for pancreatic cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Pancreatic cancer is a significant global health challenge.
- Aberrant expression of long noncoding RNAs (lncRNAs) is implicated in tumorigenesis.
- LINC00052 is a known regulator in various cancers, but its role in pancreatic cancer remains unclear.
Purpose of the Study:
- To investigate the specific mechanism and role of LINC00052 in pancreatic cancer progression.
- To explore the potential of LINC00052 as a therapeutic target for pancreatic cancer.
Main Methods:
- Quantitative analysis of LINC00052 expression in pancreatic cancer cell lines.
- In vitro assays assessing cell proliferation, apoptosis, cell cycle, migration, and invasion upon LINC00052 manipulation.
- Luciferase reporter and RNA Immunoprecipitation (RIP) assays to confirm the interaction between LINC00052 and miR-330-3p.
- In vivo studies evaluating the effect of LINC00052 on pancreatic tumor growth.
Main Results:
- LINC00052 expression was significantly downregulated in pancreatic cancer cell lines.
- Overexpression of LINC00052 suppressed proliferation, induced apoptosis, arrested the cell cycle at G1 phase, and inhibited migration and invasion in pancreatic cancer cells.
- LINC00052 directly targets and downregulates miR-330-3p, which is upregulated in pancreatic cancer.
- Inhibition of miR-330-3p counteracted the tumor-suppressive effects of LINC00052, while its overexpression promoted cancer progression.
- LINC00052 suppressed pancreatic tumor growth in vivo by modulating miR-330-3p.
Conclusions:
- LINC00052 functions as a tumor suppressor in pancreatic cancer.
- The LINC00052/miR-330-3p axis plays a critical role in regulating pancreatic cancer progression.
- LINC00052 holds promise as a potential therapeutic agent for pancreatic cancer.
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