Histology and histopathology Vol.38, nº7 (2023)
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- PublicationOpen AccessCirc_0007385 promotes the proliferation and inhibits the apoptosis of non-small cell lung cancer cells via miR-337-3p-dependent regulation of LMO3(Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Wei, Mingchao; Yin, Rongjiang; Qu, Li; Tang, JianBackground. This study intended to analyze the expression characteristic, functions and underlying mechanism of circular RNA_0007385 (circ_0007385) in non-small cell lung cancer (NSCLC). Methods and Results. RNA and protein expression was examined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assay. Cell counting kit 8 (CCK8) assay, colony formation assay, 5- Ethynyl-2’-deoxyuridine (EdU) assay and flow cytometry were applied to analyze cell proliferation ability. Flow cytometry was also conducted to assess cell apoptosis. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the predicted target relationships. Xenograft tumor model was utilized to analyze the function of circ_0007385 in vivo, and immunohistochemistry (IHC) assay was used to analyze protein expression in xenograft tumor tissues. Circ_0007385 expression was notably enhanced in NSCLC tissues and cell lines. Circ_0007385 facilitated the proliferation but suppressed the apoptosis of NSCLC cells. Circ_0007385 acted as a sponge for microRNA-337-3p (miR-337-3p), and circ_0007385 overexpression-mediated effects were largely overturned by the overexpression of miR-337-3p in NSCLC cells. MiR-337-3p interacted with the 3’ untranslated region (3’UTR) of LIM-only protein 3 (LMO3). Circ_0007385 up-regulated LMO3 level by absorbing miR-337-3p in NSCLC cells. LMO3 overexpression largely reversed miR-337-3p overexpression-induced influences in NSCLC cells. Circ_0007385 knockdown significantly restrained the growth of xenograft tumors in vivo. Conclusion. Circ_0007385 promoted the proliferation ability and inhibited the apoptosis of NSCLC cells by binding to miR-337-3p to induce LMO3 expression.
- PublicationOpen AccessCircTADA2A Up-regulates MAPK8 by targeting MiR-214-3p and recruiting EIF4A3 to promote the invasion and migration of non-small cell lung cancer cells(Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Zhang, Xi; Lei, Guangyan; Zhao, Kun; Zhang, Xinwei; Dang, ChengxueBackground. Non-small cell lung cancer (NSCLC) occupies 87% of all lung cancer cases. Due to delayed diagnosis, the prognosis of NSCLC is unfavorable. To improve the survival of patients with NSCLC, more effective therapeutic targets urgently need to be identified. Recently, circular RNAs (circRNAs) have been revealed to play a crucial role in NSCLC progression. Purpose. This research focused on the influence of circTADA2A on the malignant phenotype of NSCLC cells and its in-depth regulatory mechanisms. Methods. RT-qPCR and western blot assays were done to examine the level of gene/protein of interest. Wound healing and transwell assays were conducted to monitor the migration and invasion of NSCLC cells. Bioinformatics tools and mechanistic assays were utilized to delve into the underlying mechanism of circTADA2A in NSCLC cells. Results. The results demonstrated that circTADA2A presented a high expression in NSCLC. CircTADA2A knockdown was revealed to hamper migration and invasion of NSCLC cells. Mechanistically, circTADA2A elevated MAPK8 expression through sequestering miR214-3p and recruiting EIF4A3. Conclusion. CircTADA2A enhances MAPK8 expression by serving as a miR-214-3p sponge and EIF4A3 decoy, consequently promoting invasion and migration of NSCLC cells.
- PublicationOpen AccessUpregulation of NUAK2: A novel prognostic marker in breast cancer(Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Chen, Baorong; Wang, Bangyu; Xu, Xiongjun; Chen, Xiaopeng; Yi, Wei; Xu, Shilei; Wang, JianiBackground. Breast cancer is the most commonly diagnosed neoplasm in women worldwide. New molecular biomarkers and effective prognostic models are being developed. This study aimed to investigate the clinical and prognostic significance of NUAK2 expression in patients with breast cancer. Methods. The expression of NUAK 2 was examined in breast cancer cells and tissues by real-time PCR, western blotting, and immunohistochemical staining. CCK-8 and colony formation assays were performed to verify the effect of NUAK2 on the proliferation and tumor progression of breast cancer cells. A tumor formation assay in nude mice was performed to analyze the effect of NUAK2 on the tumorigenicity of breast cancer cells. Results. The expression of NUAK2 in breast cancer tissues was higher than that in paracarcinoma and normal breast tissues. The overall survival of patients with high NUAK2 expression was significantly lower than that of patients with low NUAK2 expression. Multivariate analyses indicated that NUAK2 was an independent prognostic indicator of survival in breast cancer. In vitro experiments demonstrated that knocking down NUAK2 in breast cancer cells inhibited cell proliferation and tumor-forming ability, and overexpression of NUAK2 showed the opposite effects. NUAK2 overexpression promoted the tumorigenicity of breast cancer cells in vivo. Conclusion. These findings suggest that NUAK2 is involved in breast cancer development and progression. NUAK2 may be a valuable prognostic indicator in patients with breast cancer.
- PublicationOpen AccessLncRNA CERS6-AS1, sponging miR-6838-5p, promotes proliferation and invasion in cervical carcinoma cells by upregulating FOXP2(Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Yan, Kun; Hu, Chunyan; Liu, Chen; Chu, Guanghua; Wang, Xinru; Ma, Shuyun; Li, LongCervical cancer (CC) is a common disease in women characterized by high recurrence rate. LncRNA ceramide synthase 6 antisense RNA 1 (CERS6-AS1) has been found to play a crucial role in the progression of breast cancer and pancreatic cancer. Nevertheless, the regulatory role of CERS6-AS1 in CC remains largely unclear. Here, we found that the expression of CERS6- AS1 was upregulated in CC tissues and cell lines compared with adjacent tissues and normal human cervical epithelial cells. CERS6-AS1 overexpression promoted proliferation and invasion, and inhibited apoptosis in CC cells, while silencing of CERS6-AS1 led to the opposite results. CERS6-AS1 was verified as a sponge of miR-6838-5p by RNA pull-down and luciferase reporter gene assays. Functional investigations revealed that CERS6-AS1 knockdown inhibited proliferation and invasion, and promoted apoptosis in CC cells, which was reversed by miR-6838-5p inhibitor. Furthermore, forkhead box P2 (FOXP2) was identified as a target for miR-6838-5p, and overexpression of miR6838-5p decreased the expression level of FOXP2. Besides, CERS6-AS1 was able to sponge miR-6838-5p to accelerate CC cell proliferation and invasion and inhibited cell apoptosis through upregulating FOXP2 expression. In general, CERS6-AS1 was able to regulate CC cell proliferation, invasion and apoptosis by the miR-6838-5p/FOXP2 axis, which suggested that CERS6-AS1 may be a potential target for the treatment of CC.
- PublicationOpen AccessHypomethylation-mediated overexpression of ITGA2 stimulates cell invasion and migration of thyroid carcinoma(Universidad de Murcia. Servicio de publicaciones, 2023) Chen, Hong; Zhang, Chunying; Li, Yanbing; Chen, ChunyouObjective. To study the molecular mechanism of DNA methylation-mediated ITGA2 overexpression in thyroid carcinoma (TC). Methods. First, 450K methylation data and mRNA expression profiles in TCGA-THCA dataset were downloaded from TCGA database. ITGA2 was identified as a methylation-driven gene by using R package “MethylMix”. Afterwards, qRT-PCR, western blot and flow cytometry assay were performed to measure ITGA2 expression in TC cells. Methylationspecific PCR was utilized to measure promoter region methylation of ITGA2 in TC cells. Transwell and wound healing assays were carried out to assess cell invasive and migratory properties. Results. Compared with normal cells, TC cells presented significantly increased ITGA2 expression. In addition, ITGA2 expression was controlled by DNA methylation. Hypomethylation of CpG island resulted in an increased ITGA2 expression. Hence, methylation and expression levels of ITGA2 were inversely associated. Moreover, overexpression of ITGA2 and promoter region hypomethylation facilitated cell invasive and migratory abilities in TC. Conclusion. These findings authenticated that promoter region hypomethylation of ITGA2 fostered ITGA2 expression as well as TC cell invasion and migration.