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Published on: August 12, 2015
Effect of silencing CITED1 gene to regulate PI3K/AKT pathway on the biological function of PTC cells and its
Wanzhi Chen1, Jichun Yu2, Rong Xie3
1Department of Thyroid Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China. Chenwanzhi111@163.com.
Abstract:
This study aims to investigate the effect of silencing the CITED1 gene to regulate the PI3K/AKT pathway on the biological function of papillary thyroid carcinoma (PTC) cells and its mechanism of action. Human PTC cells SW1736 were divided into 4 groups: control group, siCITED1 group, LY294002 group and siCITED1+LY294002 group. CITED1 was silenced by transfection with siCITED1 plasmid. The PI3K/AKT pathway was inhibited by LY294002 (5 μmmol/L). Each group was determined for cell proliferation, apoptosis and invasion capabilities, as well as PI3K/AKT transcription and protein expression levels. CITED1 mRNA and protein levels in the siCITED1 group and the siCITED1+LY294002 group were significantly lower than those in the control group (P < 0.05), and the two levels were not significantly different between the LY294002 group and the control group (P > 0.05). Compared with the control group, the siCITED1 group showed remarkably lower proliferation and invasion capabilities, and remarkably higher apoptosis rate (P < 0.05). There was no significant difference in proliferation, apoptosis and invasion capabilities between the LY294002 group and the siCITED1+LY294002 group (P > 0.05), both of which had significantly lower proliferation and invasion capabilities but significantly higher apoptosis rate than the siCITED1 group (P < 0.05). PI3K and AKT protein levels in the siCITED1 group were significantly lower than those in the control group (P < 0.05). The PI3K and AKT protein levels in the LY294002 group and the siCITED1+LY294002 group were not significantly different (P > 0.05), and were significantly lower than those in the siCITED1 group (P < 0.05). In conclusion: CITED1 silence may inhibit the progression of PTC cells by inhibiting the PI3K/AKT pathway.
Insights
Silencing the CITED1 gene inhibits papillary thyroid carcinoma (PTC) cell progression by regulating the PI3K/AKT pathway. This leads to reduced cell proliferation and invasion, alongside increased apoptosis in PTC cells.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Papillary thyroid carcinoma (PTC) is a common endocrine malignancy.
- The PI3K/AKT signaling pathway plays a crucial role in cell growth, survival, and invasion in various cancers, including PTC.
- The role of the CITED1 gene in PTC progression and its interaction with the PI3K/AKT pathway requires further elucidation.
Purpose of the Study:
- To investigate the effect of CITED1 gene silencing on the biological functions of human PTC cells.
- To determine the mechanism by which CITED1 regulates the PI3K/AKT pathway in PTC.
- To assess the impact of CITED1 silencing on cell proliferation, apoptosis, and invasion in PTC.
Main Methods:
- Human PTC SW1736 cells were utilized and divided into control, siCITED1, LY294002 (PI3K/AKT inhibitor), and combined treatment groups.
- CITED1 gene silencing was achieved via siCITED1 plasmid transfection.
- Cell proliferation, apoptosis, invasion, and PI3K/AKT pathway protein/mRNA expression levels were analyzed.
Main Results:
- Silencing CITED1 significantly decreased PTC cell proliferation and invasion while increasing apoptosis.
- Inhibition of the PI3K/AKT pathway with LY294002 also reduced proliferation and invasion and increased apoptosis.
- CITED1 silencing led to decreased PI3K and AKT protein expression, suggesting pathway regulation.
Conclusions:
- CITED1 gene silencing effectively inhibits the progression of papillary thyroid carcinoma cells.
- The inhibitory effect is mediated through the downregulation of the PI3K/AKT signaling pathway.
- Targeting CITED1 represents a potential therapeutic strategy for PTC.
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