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Transcriptome sequencing analysis reveals unique and shared antitumor effects of three statins in pancreatic cancer
Cheng Chen1, Hongjin Wu1, Deshengyue Kong2
1The NHC Key Laboratory of Drug Addiction Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China.
Abstract:
Statins, a class of commonly prescribed cholesterol‑lowering medications, have been revealed to influence the risk of multiple types of cancer. However, the antitumor effects of statins on pancreatic cancer and their differential efficacy among a variety of statins are not currently well‑defined. The aim of the present study was therefore to identify and compare the genes and related biological pathways that were affected by each individual statin on pancreatic cancer. Two human pancreatic cancer cell lines, MiaPaCa2 and PANC1, were exposed to three statins, lovastatin, fluvastatin and simvastatin. The inhibitory effect of statins on pancreatic cancer cell proliferation was first validated. Next, RNA‑seq analysis was used to determine the gene expression alterations in either low (2 µM) or high (20 µM) statin concentration‑treated cancer cells. Marked differences in gene transcription profiles of both pancreatic cancer cell lines exposed to high concentration statins were observed. Notably, the high concentration statins significantly suppressed core‑gene CCNA2‑associated cell cycle and DNA replication pathways and upregulated genes involved in ribosome and autophagy pathways. However, the low concentration statin‑induced gene expression alterations were only detected in MiaPaCa2 cells. In conclusion, a marked difference in the intra and inter cell‑type performance of pancreatic cancer cells exposed to a variety of statins at low or high concentrations was reported herein, which may provide insights for the potential clinical use of statins in future pancreatic cancer therapeutics.
Insights
Statins show varied effects on pancreatic cancer cells, suppressing cell cycle and DNA replication at high doses. Low doses only impacted one cell line, suggesting differential efficacy for potential cancer therapeutics.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Statins are widely used cholesterol-lowering drugs with potential anticancer effects.
- The specific impact of different statins on pancreatic cancer remains unclear.
- Understanding statin-induced gene expression changes is crucial for therapeutic development.
Purpose of the Study:
- To investigate and compare the effects of individual statins on pancreatic cancer cells.
- To identify specific genes and biological pathways influenced by statins.
- To assess differential statin efficacy in pancreatic cancer models.
Main Methods:
- Utilized two human pancreatic cancer cell lines (MiaPaCa2 and PANC1).
- Treated cells with lovastatin, fluvastatin, and simvastatin at low (2 µM) and high (20 µM) concentrations.
- Performed RNA-sequencing (RNA-seq) to analyze gene expression alterations.
Main Results:
- High statin concentrations significantly altered gene transcription profiles in both cell lines.
- Key findings include suppression of CCNA2-associated cell cycle and DNA replication pathways.
- Upregulation of ribosome and autophagy pathways was observed at high statin concentrations.
- Low statin concentrations induced gene expression changes only in MiaPaCa2 cells, indicating cell-type specificity.
Conclusions:
- Pancreatic cancer cells exhibit distinct responses to various statins at different concentrations.
- High-dose statins impact core cell cycle and DNA replication pathways.
- Findings suggest potential for statins in pancreatic cancer treatment, warranting further investigation.
