Histology and histopathology Vol.38, nº5 (2023)
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- PublicationOpen AccessHsa_circ_0093741 competes with FRS2 for miR-562 binding sites to promote nephroblastoma progression(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Yong, Jiang; He, Jun; Ning, FengBackground. Circular RNA (circRNA) has been shown to play an essential role in cancer progression, including nephroblastoma. Hsa_circ_ 0093741 was discovered to be highly expressed in nephroblastoma. However, its function and mechanism in nephroblastoma development are still vague. Methods. The expression levels of hsa_circ_ 0093741, miR-562 and FRS2 (Fibroblast Growth Factor Receptor Substrate 2) were detected using western blotting and quantitative real-time polymerase chain reaction. Functional experiments were performed by using cell counting kit-8, colony formation, 5-ethynyl2’-deoxyuridine (EdU), transwell, scratch assays in vitro and animal experiments in vivo. The interaction analysis was conducted using dual-luciferase reporter assay and RIP assay. Results. Hsa_circ_0093741 was highly expressed in nephroblastoma tissues and cells. Functionally, hsa_circ_0093741 silencing significantly suppressed the growth, invasion, and migration of nephroblastoma cells in vitro. MiR-562 was decreased in nephroblastoma, and was validated to be a target of hsa_circ_0093741. Inhibition of miR-562 reversed the anticancer functions of hsa_circ_0093741 silencing on nephroblastoma cells. FRS2 expression was increased in nephroblastoma and served as a target of miR-562, moreover, FRS2 overexpression attenuated the inhibitory functions of miR-562 on the nephroblastoma cell malignant phenotypes mentioned above. Pre-clinically, lentivirusmediated hsa_circ_0093741 silencing also impeded nephroblastoma tumor growth and metastasis in vivo. Conclusion. Knockdown of hsa_circ_0093741 suppresses nephroblastoma cell growth, migration and invasion by regulating the miR-562/FRS2 axis, suggesting the potential involvement of hsa_circ_0093741 in nephroblastoma progression.
- PublicationOpen AccessCircKCNQ5 controls proliferation, migration, invasion, apoptosis, and glycolysis of multiple myeloma cells by modulating miR-335-5p/BRD4 axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Li, Yan; Wang, Liang; Zhang, Nan; Xu, YanBackground. Circular RNAs (circRNAs) are key players in tumorigenesis progression. However, the role and molecular mechanisms of circKCNQ5 in multiple myeloma (MM) progression remain unclear. Methods. The quantitative real-time polymerase chain reaction was used for examining circKCNQ5, miR-335-5p, and Bromodomain-containing protein 4 (BRD4) levels. The proliferation ability of MM cells was determined by Cell Counting Kit-8 and colonyforming assays. The migration and invasion were analyzed by transwell assay. Flow cytometry was used to assess cell apoptosis. The lactate production, glucose consumption, and ATP/ADP ratios were determined by commercialized kits. The protein levels were quantified by western blot analysis. The interactions between circKCNQ5 and miR-335-5p, along with miR-335-5p and BRD4 were analyzed by dual-luciferase reporter and RNA immunoprecipitation assays. Results. The overexpression of circKCNQ5 was confirmed in MM tissues and cells. Importantly, knockdown of circKCNQ5 suppressed proliferation, migration, invasion, and glycolysis while it increased apoptosis of MM cells in vitro. Interestingly, the downregulation of miR-335-5p was able to rescue the circKCNQ5 inhibition-induced effects on MM cells. MiR-335-5p interacted with circKCNQ5, and was able to target BRD4 in MM cells. MiR-335-5p upregulation inhibited malignant phenotypes of MM cells depending on BRD4. Conclusion. CircKCNQ5 was found to stimulate MM progression through competitively sponging to miR-335-5p.
- PublicationOpen AccessCircular RNA hsa_circ_0003892 promotes the development of papillary thyroid carcinoma by regulating the miR-326/LASP1 axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Han, Peng; Liu, Junsong; Zhao, Qian; Li, Honghui; Zhang, Ting; Li, Baiya; Niu, XiaorongBackground. Thyroid cancer is the most common malignancy of the endocrine system. Circular RNA (circRNA) is recognized as a key regulator of tumorigenesis in papillary thyroid carcinoma (PTC). Here this work focused on the mechanism of circRNA_0003892 (circ_0003892) in PTC progression. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine circ_0003892, microRNA-326 (miR-326) and LIM and SH3 protein 1 (LASP1) mRNA expression levels in PTC tissues and cell lines. Besides, cell counting kit-8 (CCK-8), EdU and transwell assays were conducted to detect the proliferative, migrative and invasive abilities of PTC cells, respectively. B The targeting relationships between miR-326 and circ_0003892 or LASP1 3'-UTR were verified by dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay. Results. Circ_0003892 expression was raised in PTC tissues and cells, which was significantly interrelated with larger tumor size and extrathyroidal extension in PTC sufferers. Overexpression of circ_0003892 significantly promoted the malignant biological behaviors of PTC cells. Additionally, miR-326 was a downstream target of circ_0003892, and miR-326 overexpression weakened the promoting effect of circ_0003892 overexpression on the malignant progression of PTC. MiR-326 specifically inhibited LASP1. Circ_0003892 positively regulated LASP1 expression by targeting miR-326. Conclusion. Circ_0003892 up-regulates LASP1 expression and facilitates PTC progression via competitively binding to miR-326.
- PublicationOpen AccessMiR-29c-3p represses gastric cancer development via modulating MEST(2023) Li, Honghai; Lv, Jieqing; Wang, Jindao; Wang, Haifeng; Luo, LiangGastric cancer (GC) triggers a great number of deaths worldwide. Although great efforts have been made in treating this cancer, GC patients’ survival rate remains unsatisfactory. An increasing amount of evidence indicates that miR-29c-3p inhibits cancer progression. However, the mechanism of miR-29c-3p in GC remains to be fully defined. Hence, this work aimed to analyze the underlying mechanism of miR-29c-3p in GC. Outcomes showed marked downregulation of miR29c-3p in GC tissue and cell lines. Functional experiments exhibited that miR-29c-3p repressed GC cell malignant behaviors. Moreover, bioinformatics analysis and dual-luciferase reporter gene detection indicated that MEST was targeted by miR-29c-3p. Rescue assay further proved that MEST participated in functions of miR-29c-3p in GC. To sum up, miR-29c3p/MEST signaling pathway suppressed formation of malignant phenotypes of GC, and targeting the signaling pathway may be a new method for treating GC.
- PublicationOpen AccessCirc_0085616 contributes to the radio-resistance and progression of cervical cancer by targeting miR-541-3p/ARL2 signaling(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Tang, Yan; Zhou, Lei; Liu, LiliBackground. Circular RNAs (circRNAs) play crucial regulatory roles in cancer progression and the development of radio-resistance. Here, we intended to explore the role of circ_0085616 in cervical cancer progression and its associated mechanism. Methods. Colony formation assay was employed to analyze the radio-resistance and proliferation of cervical cancer cells. Cell proliferation ability was also assessed by 5-ethynyl-2’-deoxyuridine (EdU) assay. Cell apoptosis was analyzed by flow cytometry. Tube formation assay was performed to analyze cell angiogenesis ability. Transwell assays were conducted to measure cell migration and invasion abilities. Dualluciferase reporter assay was utilized to verify the target relationships. Xenograft mice model was used to analyze the role of circ_0085616 in tumor growth in vivo. Results. Circ_0085616 expression was elevated in cervical cancer tissues and cell lines. Circ_0085616 interference suppressed the radio-resistance, proliferation, tube formation, migration, and invasion and elevated the apoptosis rate of cervical cancer cells. Circ_0085616 acted as a sponge for microRNA-541-3p (miR-541-3p), and miR-541-3p was negatively regulated by circ_0085616 in cervical cancer cells. Circ_0085616 absence-induced changes in the behaviors of cervical cancer cells were largely overturned by anti-miR-541- 3p. miR-541-3p negatively regulated ADP ribosylation factor like GTPase 2 (ARL2) expression by binding to its 3’ untranslated region (3’UTR). miR-541-3p mimicinduced effects were largely reversed by pcDNA-ARL2 in cervical cancer cells. Circ_0085616 positively regulated ARL2 expression by sequestering miR-541-3p. Circ_0085616 absence significantly inhibited the tumor growth in vivo. Conclusion. Circ_0085616 contributed to the radioresistance and progression of cervical cancer partly through mediating the miR-541-3p/ARL2 axis.