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Anlotinib Exerts Inhibitory Effects against Cisplatin-Resistant Ovarian Cancer In Vitro and In Vivo
Yurou Ji1,2, Xinyu Li1,2, Yue Qi1,2
1Clinical School of Obstetrics and Gynecology Center, Tianjin Medical University, Tianjin 300100, China.
Abstract:
Background: Anlotinib is a highly potent multi-target tyrosine kinase inhibitor. Accumulating evidence suggests that anlotinib exhibits effective anti-tumor activity against various cancer subtypes. However, the effects of anlotinib against cisplatin-resistant (CIS) ovarian cancer (OC) are yet to be elucidated. The objective of this study was to investigate the inhibitory effect of anlotinib on the pathogenesis of cisplatin-resistant OC. Materials and Methods: Human OC cell lines (A2780 and A2780 CIS) were cultured and treated with or without anlotinib. The effects of anlotinib on cell proliferation were determined using cell-counting kit-8 and colony-formation assays. To evaluate the invasion and metastasis of OC cells, we performed wound-healing and transwell assays. The cell cycle was analyzed via flow cytometry. A xenograft mouse model was used to conduct in vivo studies to verify the effects of anlotinib. The expression of Ki-67 in the tumor tissue was detected via immunohistochemistry. Quantitative real-time polymerase chain reaction and Western blotting were used to measure the mRNA and protein levels. Results: Our study revealed that anlotinib significantly inhibited the proliferation, migration, and invasion of A2780 and A2780 CIS in a dose-dependent way in vitro (p < 0.05). Through R software ‘limma’ package analysis of GSE15372, it was found that, in comparison with A2780, PLK2 was expressed in significantly low levels in the corresponding cisplatin-resistant strains. The ERK1/2/Plk2 signaling axis mediates the inhibitory effect of anlotinib on the proliferation and migration of ovarian cancer cell lines. Moreover, our research found that anlotinib effectively inhibited the growth of tumor cells in an OC xenograft mouse model. Conclusions: In this study, anlotinib showed excellent inhibitory effects against cisplatin-resistant OC both in vitro and in vivo. These results add to the growing body of evidence supporting anlotinib as a potential anticancer agent against OC.
Insights
Anlotinib effectively inhibits cisplatin-resistant ovarian cancer (OC) by reducing proliferation and migration. This multi-target tyrosine kinase inhibitor shows promise as an anticancer agent for ovarian cancer treatment.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Anlotinib is a potent multi-target tyrosine kinase inhibitor with demonstrated anti-tumor activity.
- Cisplatin-resistant ovarian cancer (OC) remains a clinical challenge with limited treatment options.
- The efficacy of anlotinib against cisplatin-resistant OC has not been fully elucidated.
Purpose of the Study:
- To investigate the inhibitory effect of anlotinib on the pathogenesis of cisplatin-resistant ovarian cancer (OC).
- To evaluate anlotinib's impact on OC cell proliferation, invasion, and metastasis in vitro and in vivo.
Main Methods:
- In vitro studies utilized human OC cell lines (A2780 and A2780 CIS) treated with anlotinib.
- Cell proliferation, invasion, metastasis, and cell cycle were assessed using CCK-8, colony formation, wound-healing, Transwell, and flow cytometry assays.
- In vivo efficacy was evaluated in a xenograft mouse model, with Ki-67 expression analyzed via immunohistochemistry.
Main Results:
- Anlotinib significantly inhibited OC cell proliferation, migration, and invasion in a dose-dependent manner (p < 0.05).
- Analysis revealed significantly lower PLK2 expression in cisplatin-resistant OC strains compared to sensitive ones.
- The ERK1/2/Plk2 signaling axis was identified as mediating anlotinib's inhibitory effects on OC cell proliferation and migration.
Conclusions:
- Anlotinib demonstrates significant inhibitory effects against cisplatin-resistant ovarian cancer both in vitro and in vivo.
- These findings support anlotinib as a potential therapeutic agent for treating cisplatin-resistant OC.
- Further research into the ERK1/2/Plk2 pathway could offer novel therapeutic strategies for OC.
