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Ginsenoside Rg3 inhibits cell growth, migration and invasion in Caco-2 cells by downregulation of lncRNA CCAT1
1Department of Anorectal Surgery, Jining No.1 People's Hospital, Jining 272011, China; Affiliated Jining No.1 People's Hospital of Jining Medical University, Jining Medical University, Jining 272067, China.
Background:
Colorectal cancer (CRC) is a troublesome disease with high morbidity and mortality. Ginsenoside Rg3 possesses anti-cancer properties. Colon Cancer Associated Transcript 1 (CCAT1) participates in the genesis, development, invasion and metastasis of colorectal cancer. In our study, we explored the effects of Rg3 on CRC cell line Caco-2 by regulating CCAT1.
Methods:
CRC tissue was obtained from hospital and Caco-2 cells were purchased. Caco-2 cells were treated with Rg3 and/or transfected with pc- CCAT1 or pcDNA3.1. The group without Rg3 treatment was treated as control. Cell viability, cell apoptosis, cell migration and invasion were detected by Cell Counting Kit-8 assay, flow cytometry and Transwell chamber migration/invasion assay, respectively. The expression of CyclinD1, apoptosis related proteins (p53, Bcl-2, Bax, pro-/Cleaved-Caspase-3), migration and invasion related proteins (MMP-9 and vimentin), and phosphatidylinositol 3'-kinase (PI3K)/protein kinase B (AKT) related proteins (p/t-PI3K, p/t-AKT) were examined by western blot. The expression of CCAT1 was measured by quantitative real time RCR (qRT-PCR).
Results:
Rg3 significantly decreased cell viability, migration and invasion, and promoted apoptosis. Meanwhile, the expression of Cyclin D1, matrix metalloproteinase (MMP)-9 and vimentin was downregulated. The expression of apoptosis-related proteins p53, Bax, and Cleaved-Caspase-3 were upregulated while Bcl-2 was downregulated by the treatment of Rg3 compared with control. Furthermore, CCAT1 was upregulated in CRC tissue and Rg3 negatively regulated CCAT1 expression. Transfection with pc-CCAT1 led to the opposite results as compared with transfection with pcDNA3.1 in Rg3 treated cells. In addition, Rg3 decreased the phosphorylation of PI3K and AKT.
Conclusion:
Ginsenoside Rg3 inhibits migration and invasion, and promotes apoptosis of Caco-2 cells by suppression expression of LncRNA CCAT1.
Insights
Ginsenoside Rg3 inhibits colorectal cancer (CRC) cell growth and metastasis by downregulating CCAT1. This study shows Rg3
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Colorectal cancer (CRC) presents significant global health challenges with high morbidity and mortality.
- Ginsenoside Rg3, a compound derived from ginseng, exhibits promising anti-cancer properties.
- Colon Cancer Associated Transcript 1 (CCAT1) is implicated in the progression, invasion, and metastasis of CRC.
Purpose of the Study:
- To investigate the anti-cancer effects of Ginsenoside Rg3 on the Caco-2 colorectal cancer cell line.
- To elucidate the role of CCAT1 in mediating the effects of Ginsenoside Rg3 in CRC.
Main Methods:
- Caco-2 cells were treated with Ginsenoside Rg3 and/or transfected with CCAT1 expression vectors.
- Cell viability, apoptosis, migration, and invasion were assessed using standard assays (CCK-8, flow cytometry, Transwell).
- Protein and RNA expression levels of key molecules (e.g., Cyclin D1, apoptosis markers, MMP-9, PI3K/AKT pathway, CCAT1) were analyzed via Western blot and qRT-PCR.
Main Results:
- Ginsenoside Rg3 significantly reduced Caco-2 cell viability, migration, and invasion while promoting apoptosis.
- Rg3 treatment downregulated Cyclin D1, MMP-9, and vimentin, and modulated apoptosis-related proteins (p53, Bcl-2, Bax, Caspase-3).
- CCAT1 expression was elevated in CRC tissues and negatively regulated by Rg3; CCAT1 overexpression counteracted Rg3's inhibitory effects.
Conclusions:
- Ginsenoside Rg3 demonstrates potent anti-cancer activity against Caco-2 cells.
- The anti-cancer effects of Rg3 are mediated, in part, through the suppression of CCAT1 expression.
- Rg3 inhibits CRC cell migration and invasion and promotes apoptosis by downregulating CCAT1, suggesting therapeutic potential.
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