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Background and purpose: Circular RNA (circRNA) plays an important regulatory role in the development of a variety of tumors. However, the abnormal expression and biological function of circRNA in nasopharyngeal carcinoma remain unclear. This study aimed to explore the effect of hsa_circ_0012779 on the biological behavior of nasopharyngeal carcinoma cells and its molecular mechanism. Methods: The expression of hsa_circ_0012779 in human immortalized nasopharyngeal epithelial cell line NP69 and nasopharyngeal carcinoma cell lines CNE2, 5-8F, HNE1 and SUNE1 was detected by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR). Cell counting kit-8 (CCK-8) assay and transwell invasion assay were used to detect the effect of hsa_circ_0012779 on the proliferation and invasion ability of nasopharyngeal carcinoma cells. The protein level of ELAV like protein 1 (ELAVL1) in NPC cells with hsa_circ_0012779 knockdown was detected by Western blot. The binding of hsa_circ_0012779 and ELAVL1 was verified by RNA pull-down assay. Results: hsa_circ_0012779 was highly expressed in nasopharyngeal carcinoma tissues and cells. Knockdown hsa_circ_0012779 could inhibit the proliferation and invasion of nasopharyngeal carcinoma cells. hsa_circ_0012779 bound to RNA-binding protein ELAVL1 to promote its expression and colocalization in cytoplasm. In the meanwhile, the effect of knockdown hsa_circ_0012779 on nasopharyngeal carcinoma cells could be reversed by the overexpression of ELAVL1. Conclusion: hsa_circ_0012779 promote the expression of ELAVL1 and thus promote the proliferation and invasion of nasopharyngeal carcinoma, and influence the occurrence and development of nasopharyngeal carcinoma.

Background: In recent years, the development of high‐throughput sequencing technology has promoted the rapid development of circRNA‐related research. Studies have found that circRNA plays a key role in a variety of tumors, but few people study the role of circRNA in nasopharyngeal carcinoma. Under comprehensive treatments, the 5‐year survival rate can reach about 70%, but some patients still have distant metastases or recurrences after treatment. Therefore, it is very important to study the molecular mechanisms of the proliferation and invasion of nasopharyngeal carcinoma. Methods: QRT‐PCR was applied to detect the relative expression level of circFOXM1 in NPC and nasopharyngeal epithelial cell lines. We knocked down circFOXM1 and studied the influence of circFOXM1 on NPC cells. Nuclear and cytoplasmic RNA isolation experiments, fluorescence in situ hybridization (FISH), bioinformatics analysis, the dual‐luciferase reporter experiment, Western Blot, and other experiments were conducted to verify the relationships among circFOXM1, miR‐136‐5p, and SMAD2. We collected clinical NPC samples to prove the effect of circFOXM1 on the prognosis and treatment of NPC. Results: In this study, we found that circFOXM1 is highly expressed in nasopharyngeal carcinoma tissue cells compared with adjacent normal tissues and is related to the staging of nasopharyngeal carcinoma. High expression of circFOXM1 indicates a poor prognosis for nasopharyngeal carcinoma. Knockdown of CircFOXM1 inhibited the proliferation and invasion of nasopharyngeal carcinoma cells. Conclusion: CircFOXM1 promotes the malignant proliferation of nasopharyngeal carcinoma cells by regulating the miR‐136‐5p‐SMAD2 axis. [ABSTRACT FROM AUTHOR]

In China, esophageal squamous cell carcinoma (ESCC), capable of direct invasion and early metastasis, exhibits high mortality. Identification of the molecular basis driving ESCC progression and development of new diagnostic biomarkers are urgently needed. Cyclin-dependent kinase inhibitor 3 (CDKN3) performs crucial roles in the modulation of tumor development. The present study aimed to explore the functions and underlying mechanism of CDKN3 in regulating ESCC cell proliferation and invasion. The expression levels of CDKN3 in ESCC cells were evaluated by reverse transcription-quantitative PCR. Cell counting kit-8 and colony forming assays were used to evaluate cell viability. Wound-healing assay was performed to explore cell migration. Transwell invasion analysis was conducted to investigate the invasive capacity of ESCC cells. Protein levels were detected by western blot assay. The results demonstrated that the expression of CDKN3 was significantly upregulated in ESCC tissues, as predicted using the UALCAN and Gene Expression Omnibus databases. PCR and western blot assays confirmed that CDKN3 was upregulated in ESCC cell lines. Functional assays revealed that CDKN3 knockdown with small interfering RNA decreased the ability of ESCC cells to proliferate, invade and migrate and suppressed G1/S transition. Further mechanistic analyses demonstrated that CDKN3 promoted cell proliferation and invasion by activating the AKT signaling pathway in ESCC cells. To the best of our knowledge, the present study is the first to identify the functions of CDKN3 in ESCC and provide evidence that CDKN3 regulates tumor progression by activating the AKT signaling pathway. Therefore, CDKN3 may serve as a potential effective therapeutic target for ESCC treatment. [ABSTRACT FROM AUTHOR]

Background: Nasopharyngeal carcinoma (NPC) is a common malignant tumor characterized by highly malignant local invasion and distant metastasis. Recently, increasing attention has been paid to long noncoding RNAs (lncRNAs), which play significant roles in tumorigenesis and progression. However, little is known about the potential role of the lncRNA urothelial carcinoma-associated 1 (UCA1) in NPC cell invasion and migration. Methods: Real-time quantitative PCR was used to analyze the expression of lncRNA UCA1 in NPC cell lines and NP69. lncRNA UCA1 knock-down nasopharyngeal carcinoma cell line models were established through siRNA. Cell viability was evaluated by Cell counting kit-8 and Colony forming assay. The migration and invasion capacities were evaluated by wound healing and transwell migration and invasion assays. Western blot analysis were used to examine protein changes followed by UCA1 knock-down. Results: Our study confirmed that UCA1 was upregulated in NPC cell lines and involved in NPC tumorigenesis according to our established UCA1-associated competing endogenous RNA network. Moreover, functional analyses indicated that the downregulation of UCA1 exerted inhibitory effects on cell proliferation, invasion, and migration. Mechanistic analyses revealed that UCA1 was the target of miR-145 and functioned as a sponge to repress miR-145 expression. Rescue experiments suggested that lncRNA UCA1 reversed the miR-145-mediated inhibition on oncogene ADAM17 expression, thus promoting the proliferation, invasion, and migration of NPC cells. Conclusion: LncRNA UCA1 functions as a tumor promoter in NPC. UCA1 promotes the proliferation and invasion of NPC cells by sponging miR-145, functionally altering ADAM17 expression targeted by miR-145. Our exploration of the underlying mechanism of UCA1 in NPC may provide novel therapeutic targets for NPC. [ABSTRACT FROM AUTHOR]