Mancozeb (ethylene bis-dithiocarbamate) is an organometallic fungicide and is widely used in agriculture and is related to women’s spontaneous abortion and menstrual abnormalities. Bone marrow mesenchymal stem cells (BMSCs) can impede endometrial fibrosis via suppressing PI3K pathway, but its effect on the activity of endometrial cells induced by mancozeb/EDU is unclear. This study intends to explore the protective effects of co-culture with BMSCs on endometrial cells after mancozeb/EDU treatment. Endometrial cells were randomized into control group, mancozeb/EDU group (mancozeb/EDU treatment), BMSCs group (cells were co-cultured with BMSCs after mancozeb/EDU treatment), and inhibitor group (treated with PI3K-Akt-mTOR inhibitor) followed by analysis of the expression of PI3K-Akt-mTOR pathway-related proteins, cell viability by MTT and cell invasion and migration by Transwell and scratch test. Mancozeb/EDU treatment significantly inhibited PI3K-Akt-mTOR signals and cell proliferation, increased apoptosis and decreased cell invasion and migration, which were all reversed by co-culture with BMSCs. Additionally, the co-culture with BMSCs modulated the In Vitro viability of endometrial cells by influencing PI3K-Akt-mTOR signal transduction pathway, which can be inverted by PI3K-Akt-mTOR pathway-specific antagonists. In conclusion, BMSCs exerted a protective effect on the In Vitro viability of endometrial cells by manipulating the PI3K/Akt/mTOR signal transduction, which helped to protect endometrial cells from damage caused by mancozeb/ETU treatment.
Background: Circular RNAs (circRNAs) have a vital role in the occurrence of numerous cancers. However, its function and pattern of expression in cervical cancer (CC) remain unclear. This research aims to investigate the hsa_circ_000002’s regulatory mechanism in CC. Methods: Hsa_circ_0000021, miR-3940-3p, and KPNA2 expression levels were estimated through qRT-PCR. Nuclear/cytoplasmic separation was conducted to find the subcellular location of hsa_circ_0000021. Western blot was done to estimate the levels of KPNA2 protein. CCK-8, BrdU, wound healing, transwell, and tumor xenograft assays were performed to study how hsa_circ_0000021/miR-3940-3P/KPNA2 function affect CC. Hsa_circ_0000021’s targeting relationships with miR-3940-3p and KPNA2 were ascertained through RIP and luciferase experiments. Results: Hsa_circ_0000021 and KPNA2 were overexpressed and inversely associated with the levels of miR-3940-3p in CC. Knocking down either hsa_circ_0000021 or KPNA2 repressed the growth of CC tumors as well as the proliferation, invasion, and migration of CC cells. Silencing miR-3940-3p promoted the malignant proliferation of CC cells. Regarding its mechanism, hsa_circ_0000021 affected the malignant CC cell proliferation via the sponging of miR-3940-3p, which targeted KPNA2. Conclusion: Hsa_circ_0000021 regulates the miR-3940-3p/KPNA2 axis to promote CC occurrence. This potentially is a novel target for CC treatment.
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