Abstract
Objective To investigate the effects of Apatinib on the “stemness” of lung cancer cells in vivo and to explore its related mechanisms. Methods A xenograft model of lung cancer cells A549 was established in nude mice and randomized into a control group (n = 4) and an Apatinib group (n = 4). Tumor tissues were harvested after 2 weeks, and mRNA was extracted to detect changes in stemness-related genes (CD133, EPCAM, CD13, CD90, ALDH1, CD44, CD45, SOX2, NANOG, and OCT4) and Wnt/β-catenin, Hedgehog, and Hippo signal pathways. Results Compared with the control group, the volume and weight of nude mice treated with Apatinib were different and had statistical significance. Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3. Apatinib treatment also inhibited the Wnt/β-catenin, Hedgehog, and Hippo signaling pathways. Conclusion Apatinib suppressed the growth of non-small-cell lung cancer cells by repressing the stemness of lung cancer through the inhibition of the Hedgehog, Hippo, and Wnt signaling pathways.
Highlights
Lung cancer is one of the most common malignant tumors in the world
1.8 million people are diagnosed with lung cancer every year, with 1.6 million people dying from the deadly disease [1]. e 5-year survival rate for lung cancer is still less than 20%, considerable progress has been made in various treatments, such as surgery, radiotherapy, chemotherapy, and targeted therapy
Drugs were administered when the tumor volume of the nude mice in the two groups reached about 100 mm3. e body weight and tumor volume were measured and recorded on days 8, 11, 14, 17, and 20 after inoculation; the volume change curve is shown in Figure 1(a). e results indicated that the growth and volume of tumors were slower and smaller, respectively, in the Apatinib group than in the control group (P < 0.05). e final tumor masses of the two groups were compared as shown below (Figure 1(b))
Summary
To investigate the effects of Apatinib on the “stemness” of lung cancer cells in vivo and to explore its related mechanisms. A xenograft model of lung cancer cells A549 was established in nude mice and randomized into a control group (n 4) and an Apatinib group (n 4). Tumor tissues were harvested after 2 weeks, and mRNA was extracted to detect changes in stemness-related genes (CD133, EPCAM, CD13, CD90, ALDH1, CD44, CD45, SOX2, NANOG, and OCT4) and Wnt/ β-catenin, Hedgehog, and Hippo signal pathways. Apatinib treatment inhibited the Wnt/ β-catenin, Hedgehog, and Hippo signaling pathways. Apatinib suppressed the growth of non-small-cell lung cancer cells by repressing the stemness of lung cancer through the inhibition of the Hedgehog, Hippo, and Wnt signaling pathways
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