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Ropivacaine Administration Suppressed A549 Lung Adenocarcinoma Cell Proliferation and Migration via ACE2 Upregulation
Masae Iwasaki1, Makiko Yamamoto1, Masahiro Tomihari1
1Department of Anesthesiology and Pain Medicine, Graduate School of Medicine, Nippon Medical School, Tokyo 113-8602, Japan.
Background:
Previous studies have suggested that perioperative anesthesia could have direct impacts on cancer cell biology. The present study investigated the effects of ropivacaine administration on lung adenocarcinoma cells.
Methods:
Ropivacaine was administered to A549 cells at concentrations of 0.1, 1, and 6 mM for 2 h. Angiotensin-converting enzyme 2 (ACE2) small interfering RNA (siRNA) transfection was performed 6 h prior to ropivacaine administration. Cell proliferation and migration were assessed with cell counting kit 8 (CCK-8) and a wound healing assay at 0 and 24 h after anesthesia exposure. PCR arrays were performed, followed by PCR validation.
Results:
Ropivacaine administration inhibited A549 cell proliferation and migration in a concentration-dependent manner, with ACE2 upregulation and HIF1α (hypoxia-inducible factor 1α) downregulation. The anticancer effect of ropivacaine was canceled out via ACE2 siRNA transfection. PCR arrays showed specific gene change patterns in the ropivacaine and respective ACE2-knockdown groups. EGFR (epidermal growth factor receptor), BAX (Bcl-2-associated X protein) and BCL2 (B-cell/CLL lymphoma 2) were suppressed with ropivacaine administration; these effects were reversed via ACE2 siRNA induction.
Conclusion:
Ropivacaine administration inhibited A549 cell biology in conjunction with ACE2 upregulation via the inhibition of the Wnt1 (wingless/Integrated 1) pathway.
Insights
Ropivacaine, an anesthetic, inhibits lung adenocarcinoma cell proliferation and migration by upregulating angiotensin-converting enzyme 2 (ACE2). This effect was reversed when ACE2 was inhibited, suggesting a key role for ACE2 in ropivacaine
Area of Science:
- Anesthesiology
- Oncology
- Molecular Biology
Background:
- Perioperative anesthesia may influence cancer cell biology.
- The impact of ropivacaine on lung adenocarcinoma cells warrants investigation.
Purpose of the Study:
- To investigate the effects of ropivacaine on lung adenocarcinoma (A549) cell proliferation and migration.
- To elucidate the role of angiotensin-converting enzyme 2 (ACE2) in mediating these effects.
Main Methods:
- A549 cells were treated with varying concentrations of ropivacaine.
- Angiotensin-converting enzyme 2 (ACE2) small interfering RNA (siRNA) was used to inhibit ACE2 expression.
- Cell proliferation and migration were assessed using CCK-8 and wound healing assays.
- Gene expression changes were analyzed using PCR arrays and validation.
Main Results:
- Ropivacaine inhibited A549 cell proliferation and migration in a concentration-dependent manner.
- ACE2 was upregulated, and hypoxia-inducible factor 1α (HIF1α) was downregulated by ropivacaine.
- Inhibition of ACE2 reversed the anticancer effects of ropivacaine.
- Ropivacaine suppressed EGFR, BAX, and BCL2 expression, which was reversed by ACE2 siRNA.
Conclusions:
- Ropivacaine inhibits lung adenocarcinoma cell biology.
- ACE2 upregulation is crucial for ropivacaine's anticancer effects.
- The Wnt1 pathway may be involved in ropivacaine's mechanism of action.
