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Published on: April 22, 2021
Circ-RNF111 contributes to paclitaxel resistance in breast cancer by elevating E2F3 expression via miR-140-5p
Hongliang Zang1, Yuhui Li1, Xue Zhang1
1Department of General Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.
Background:
Circular RNAs (circRNAs) have been demonstrated to act as key regulators in the chemoresistance of human cancers, including breast cancer (BC). Here, we aimed to explore the role of circ-RNF111 in paclitaxel (PTX) resistance of BC.
Methods:
Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine the expression of circ-RNF111, microRNA-140-5p (miR-140-5p) and E2F transcription factor 3 (E2F3) mRNA. The half maximal inhibitory concentration (IC50 ) of PTX, cell viability, colony formation and cell invasion were assessed by cell counting kit-8 (CCK-8) assay, colony formation assay and transwell assay, respectively. Glucose consumption and lactate production were determined by specific kits. A murine xenograft model was established to investigate the role of circ-RNF111 in PTX resistance of BC in vivo. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the relationship between miR-140-5p and circ-RNF111 or E2F3. Western blot assay was conducted to examine the protein level of E2F3.
Results:
Circ-RNF111 was upregulated in PTX-resistant BC tissues and cells. Circ-RNF111 knockdown restrained IC50 of PTX, cell viability, colony numbers, cell invasion and glycolysis in PTX-resistant BC cells in vitro and enhanced PTX sensitivity in vivo. MiR-140-5p was a target of circ-RNF111 and miR-140-5p expression was negatively correlated with circ-RNF111 expression in BC tissues. The effect of circ-RNF111 knockdown on PTX resistance was rescued by miR-140-5p deletion. Additionally, miR-140-5p could interact with E2F3 and negatively regulate E2F3 expression. Moreover, miR-140-5p suppressed IC50 of PTX, cell viability, colony numbers, cell invasion and glycolysis by targeting E2F3.
Conclusions:
Circ-RNF111 improved PTX resistance of BC by upregulating E2F3 via sponging miR-140-5p.
Insights
Circular RNA-RNF111 (circ-RNF111) promotes paclitaxel resistance in breast cancer (BC) by upregulating E2F3 through microRNA-140-5p (miR-140-5p) sponging. Reducing circ-RNF111 enhances BC chemo-sensitivity.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Circular RNAs (circRNAs) are key regulators in chemoresistance of human cancers, including breast cancer (BC).
- The specific role of circ-RNF111 in paclitaxel (PTX) resistance in BC requires further investigation.
Purpose of the Study:
- To explore the function and mechanism of circ-RNF111 in paclitaxel (PTX) resistance of breast cancer (BC).
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) for gene expression analysis.
- Cell viability, invasion, and colony formation assays to assess cellular response to PTX.
- In vivo murine xenograft model to evaluate PTX resistance.
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
Main Results:
- Circ-RNF111 expression was upregulated in PTX-resistant BC tissues and cells.
- Circ-RNF111 knockdown reduced PTX resistance, cell viability, invasion, and glycolysis in vitro, and enhanced PTX sensitivity in vivo.
- Circ-RNF111 acts as a sponge for miR-140-5p, which targets and negatively regulates E2F3 expression.
Conclusions:
- Circ-RNF111 enhances BC paclitaxel resistance by upregulating E2F3 via sponging miR-140-5p.
- Targeting circ-RNF111 may represent a therapeutic strategy to overcome PTX resistance in breast cancer.
