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Published on: August 2, 2024
Circ_0000231 promotes paclitaxel resistance in ovarian cancer by regulating miR-140/RAP1B
Jiao Liu1,2, Han Wang1, Shuqin Xiao1
1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University Shenyang, Liaoning, China.
Abstract:
Circular RNAs (circRNAs) are identified as vital regulators in a variety of cancers. However, the involvement of circ_0000231 in paclitaxel (PTX) resistant ovarian cancer (OC) remains unclear. In this study, we examined the levels of circ_0000231, microRNA-140 (miR-140) and RAP1B in PTX-resistant OC tissues and cells and found that circ_0000231 and RAP1B levels were increased, while miR-140 level was decreased in these cells. Depletion of circ_0000231 could inhibit the resistance, proliferation, invasion, migration and EMT and promoted the apoptosis of PTX-resistant OC cells. The opposite effects were observed by overexpression of circ_0000231. Furthermore, the effect of circ_0000231 on the PTX sensitivity of OC cells was investigated by using xenograft tumor models, and circ_0000231 knockdown increased PTX sensitivity of OC in vivo. Mechanistically, we demonstrated that circ_0000231 acted as a sponge for miR-140, and RAP1B was the target gene of miR-140. Taken together, these data indicated that circ_0000231 was a key molecule required for the growth, migration, and PTX-resistance of OC cells and was involved in EMT. Knockdown of circ_000231 suppressed PTX-resistant OC progression via regulating miR-140/RAP1B signaling pathway. circ_0000231 might play vital roles in the tumorigenesis and chemoresistance of OC.
Insights
Circular RNA circ_0000231 promotes paclitaxel resistance in ovarian cancer by sponging miR-140 and upregulating RAP1B. Its depletion enhances chemosensitivity and inhibits tumor progression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Circular RNAs (circRNAs) are crucial in cancer development.
- The role of circ_0000231 in paclitaxel-resistant ovarian cancer (OC) is not well understood.
Purpose of the Study:
- To investigate the function and mechanism of circ_0000231 in paclitaxel-resistant ovarian cancer.
- To explore the relationship between circ_0000231, miR-140, and RAP1B in ovarian cancer chemoresistance.
Main Methods:
- Quantification of circ_0000231, miR-140, and RAP1B in PTX-resistant OC tissues and cells.
- In vitro experiments involving circ_0000231 depletion and overexpression.
- In vivo xenograft tumor models to assess PTX sensitivity.
- Mechanistic studies to elucidate the circ_0000231/miR-140/RAP1B interaction.
Main Results:
- circ_0000231 and RAP1B levels were elevated, while miR-140 was decreased in PTX-resistant OC.
- circ_0000231 knockdown inhibited proliferation, invasion, migration, EMT, and chemoresistance, while promoting apoptosis.
- circ_0000231 depletion increased PTX sensitivity in vivo.
- circ_0000231 functions as a miR-140 sponge, with RAP1B as a target of miR-140.
Conclusions:
- circ_0000231 is a key driver of ovarian cancer progression and paclitaxel resistance.
- The circ_0000231/miR-140/RAP1B axis regulates chemoresistance and tumor growth in ovarian cancer.
- circ_0000231 represents a potential therapeutic target for overcoming paclitaxel resistance in ovarian cancer.
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