Jing Shi

RETRACTED: Effect of angiogenesis inhibitors on wound healing in patients with ovarian cancer: A meta‐analysis

Abstract Angiogenic inhibitors have been demonstrated to inhibit tumour cells in ovarian carcinoma, but the initial data are not accurate enough to indicate the influence of these drugs on the post‐therapy wound healing. In order to assess the effect of angiogenic inhibitors on the treatment of wound healing in ovarian carcinoma, we performed a meta‐analysis of related literature. For this meta‐analysis, we looked up the data from 4 databases: PubMed, EMBASE, Web of Science and the Cochrane Library. All literature searches were performed up to October 2023. The ROBINS‐I tool was applied to evaluate the risk of bias in the inclusion trials, and statistical analysis was performed with RevMan 5.3. In this research, 971 related research were chosen, and 9 of them were selected. These studies were published between 2013 and 2023. In all 9 trials, a total of 3902 patients were enrolled. There was a significant reduction in the risk of wound infection in the control group than in those who received angiogenesis inhibitors (OR, 0.66; 95% CI, 0.49–0.89 p  = 0.007). The risk of developing an abscess was not significantly different from that of those who received angiogenesis inhibitors (OR, 0.80; 95% CI, 0.20–3.12 p  = 0.74). The risk of perforation in the control group was smaller than that in those receiving angiogenic inhibitors (OR, 0.25; 95% CI, 0.11–0.56 p  = 0.0006). There was a significant increase in the risk of injury and GI perforation in women who received angiogenic inhibitors than in the control group. But the incidence of abscess did not differ significantly among the two groups.

CircSMAD2 accelerates endometrial cancer cell proliferation and metastasis by regulating the miR-1277-5p/MFGE8 axis

Endometrial cancer (EC) is a common gynecological malignant tumor. CircRNAs play crucial roles in cancer progression and metastasis. However, the biological functions of circRNAs in EC remain largely unknown. CircSMAD2, miR-1277-5p, MFGE8 and relative maker protein expression in EC tissues or cell lines were analyzed by quantitative real-time polymerase chain reaction and Western blot. In vitro and in vivo functional assays, including EDU, CCK8, colony formation, transwell, tube formation and tumor xenograft assays, were conduct to explore the effects of circSMAD2 on EC. Mechanism assays were conducted to confirm the binding between miR-1277-5p and circSMAD2 or MFGE8 expression. Upregulation of circSMAD2 was uncovered in both EC tissues and cell lines. Functionally, silencing of circSMAD2 apparently inhibited the proliferation, migration, invasion and angiogenesis of EC cell lines in vitro. Mechanistically, circSMAD2 sponged miR-1277-5p to upregulate MFGE8 expression. The decrease of miR-1277-5p and increase of MFGE8 were observed both in EC tissues and cell lines. Then MFGE8 knockdown or miR-1277-5p upregulation suppressed EC cell oncogenic biological behavior. Rescue experiments showed that miR-1277-5p mimics countervailed the anticancer effects of circSMAD2 silencing on EC. Besides that, MFGE8 overexpression also attenuated the inhibitory action of miR-1277-5p mimic in EC. Moreover, knockdown of circSMAD2 inhibited EC growth in vivo. CircSMAD2 functions as an oncogene in promoting the progression of EC through miR-1277-5p/MFGE8 axis.