Circ_101341 Deteriorates the Progression of Clear Cell Renal Cell Carcinoma Through the miR- 411/EGLN3 Axis.

Cancer Manag Res

Department of Urology, Heji Hospital, Changzhi Medical College, Changzhi, Shanxi 046000, People's Republic of China.

Published: December 2020


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Background: Clear cell renal cell carcinoma (ccRCC) is one of the main subtypes of renal cell carcinoma, with intense aggressiveness. The involvement of circular RNAs (circRNAs) in human cancers attracts much concern. The intention of this study was to investigate the expression of circ_101341 and explore its function in ccRCC.

Materials And Methods: The expression of circ_101341, miR-411 and Egl nine homolog 3 () was measured using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed by cell counting kit-8 (CCK-8) assay and colony formation assay. Cell migration and invasion were monitored by transwell assay. Xenograft model was established to explore the role of circ_101341 in vivo. The protein levels of E-cadherin (E-cad), N-cadherin (N-cad), matrix metalloprotein-9 (MMP9) and EGLN3 were detected by Western blot. Bioinformatic analysis was conducted using Circinteractome and starBase. The targeted relationship was verified using dual-luciferase reporter assay, RNA-binding protein immunoprecipitation (RIP) assay and RNA pull-down assay.

Results: The expression of circ_101341 was elevated in ccRCC tissues and cells. Functionally, circ_101341 knockdown depleted proliferation, migration and invasion of ccRCC cells in vitro and restricted tumor growth in vivo. Circ_101341 directly targeted miR-411, and miR-411 inhibition revised the inhibitory effects of circ_101341 knockdown on proliferation, migration and invasion in ccRCC cells. Moreover, miR-411 directly bound to EGLN3, and overexpression also rescued the effects of circ_101341 knockdown.

Conclusion: Circ_101341 functioned as a tumor promoter to strengthen proliferation, migration and invasion by regulating via sponging miR-411, indicating that circ_101341 was a potential diagnostic and therapeutic biomarker of ccRCC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7781030PMC
http://dx.doi.org/10.2147/CMAR.S272287DOI Listing

Publication Analysis

Top Keywords

migration invasion
16
renal cell
12
cell carcinoma
12
expression circ_101341
12
proliferation migration
12
circ_101341
11
cell
8
clear cell
8
cell renal
8
circ_101341 knockdown
8

Similar Publications

Objective: This study aimed to probe the role of Shenling Baizhu powder (SLBZP) in inhibiting breast cancer (BC) lung metastasis, focusing on epithelial-to-mesenchymal transition (EMT) and ferroptosis.

Methods: BC 4T1 cells were treated with low (3.13 µg/mL) and high (12.

View Article and Find Full Text PDF

Noncoding RNA regulatory networks play crucial roles in human breast cancer. The aim of this study was to establish a network containing multi-type RNAs and RBPs in triple-negative breast cancer (TNBC). Differential expression analyses of lncRNAs, miRNAs, and genes were performed using the GEO2R tool.

View Article and Find Full Text PDF

Endoscopic vacuum therapy (EVT) offers an effective alternative for the treatment of anastomotic leakage. Current treatment options for leakage include conservative treatment, stent placement, or reoperation. However, conservative treatment often results in slow recovery and is frequently ineffective in severe cases.

View Article and Find Full Text PDF

Long non-coding RNA MALAT1 regulates epithelial-mesenchymal transition (EMT) and metastasis in epithelial ovarian cancer (EOC) through a competing endogenous RNA (ceRNA) mechanism involving miRNA modulation. This study aimed to elucidate the molecular pathway by which MALAT1 influences EMT and metastatic behavior via interaction with miR-200c-3p and SNAI2. MALAT1 expression was genetically manipulated in the EOC cell line SK-OV-3 by either overexpression or knockdown.

View Article and Find Full Text PDF

Alterations in the structure of the Golgi apparatus play a pivotal role in cancer progression and invasion. A better understanding of how Golgi morphology regulates the metastatic potential of cancer cells could help identify potential treatment strategies. In this study, we investigated how specific structural variations in the Golgi, particularly fragmentation and condensation, influence the malignancy of gastric cancer using human cell lines, xenograft mouse models, and human patient tissue samples.

View Article and Find Full Text PDF