Abstract
BackgroundRadiotherapy is a main therapeutic method for cancers, including colon cancer. In the current study, we aim to explore the effects of circular RNA (circRNA) circ_0055625 in the progression and radiosensitivity of colon cancer and the underlying mechanism.MethodsThe expression of circ_0055625 and musashi homolog 1 (MSI1) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). MSI1 protein expression was determined by Western blot. Cell proliferation was assessed by cell counting kit-8 (CCK-8) and colony formation assays. Cell survival fraction, apoptosis, and invasion were investigated by colony formation assay, flow cytometry analysis, and transwell invasion assay, respectively. Cell migration was detected by wound-healing and transwell migration assays. The binding relationship between microRNA-338-3p (miR-338-3p) and circ_0055625 or MSI1 was predicted by online databases and identified by Dual-Luciferase Reporter Assay. The effects of circ_0055625 silencing on the tumor formation and radiosensitivity of colon cancer in vivo were explored by in vivo tumor formation assay.ResultsCirc_0055625 and MSI1 were upregulated in colon cancer tissues and cells relative to control groups. Radiation treatment apparently increased the expression of circ_0055625 and MSI1 in colon cancer cells. Circ_0055625 knockdown or MSI1 silencing repressed cell proliferation, migration, and invasion and promoted cell apoptosis and radiosensitivity in colon cancer. Also, circ_0055625 silencing-mediated effects were attenuated by MSI1 overexpression. Additionally, circ_0055625 silencing reduced MSI1 expression, which could be attenuated by miR-338-3p inhibitor. Mechanically, circ_0055625 acted as a sponge for miR-338-3p to regulate MSI1. Furthermore, circ_0055625 knockdown hindered tumor growth and improved radiosensitivity in vivo.ConclusionCirc_0055625 repression inhibited the progression and radioresistance of colon cancer by downregulating MSI1 through sponging miR-338-3p. This result might provide a theoretical basis for improving the therapy of colon cancer with radiation.
Highlights
Colon cancer is one of the most commonly diagnosed digestive malignancy and poses a heavy burden to human health globally
Circ_0055625 and musashi homolog 1 (MSI1) were highly expressed in colon cancer tissues and cells with poor survival rate In order to determine the properties of circ_0055625 and MSI1 in the progression and radiosensitivity of colon cancer, their expression was firstly detected in colon cancer tissues and cells
Kaplan-Meier methods demonstrated that both high circ_0055625 and MSI1 expression were correlated with poor survival rate of colon cancer patients (Fig. 1d, e)
Summary
Colon cancer is one of the most commonly diagnosed digestive malignancy and poses a heavy burden to human health globally. More than 1,090,000 people are newly diagnosed with colon cancer every year, and about 50% of them die owing to the high rate of metastasis [1]. Clinical data reveal that the combination of operation with radiotherapy can effectively reduce the recurrence rate of colon cancer [2]. More exploration about the mechanism underlying the resistance of colon cancer to radiation is necessary to seek effective therapeutic strategy for colon cancer. Radiotherapy is a main therapeutic method for cancers, including colon cancer. We aim to explore the effects of circular RNA (circRNA) circ_0055625 in the progression and radiosensitivity of colon cancer and the underlying mechanism
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