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Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
Published on: February 8, 2020
The oncogenic effect and mechanism of LINC00520/miR-372/SLC7A11 axis in renal clear cell carcinoma
Yong-Bo Chen1,2, Liang-You Tang1, Run-Tian Luo3
1Department of Urology, People's Hospital of Deyang City, No. 173 Taishan North Road, Deyang, 618000, Sichuan, China.
Abstract:
To investigate the expression, function, and potential mechanism of long non-coding RNA LINC00520 as a competitive endogenous RNA in clear cell renal cell carcinoma (ccRCC) by regulating the miR-372/SLC7A11 axis in renal cell carcinoma progression. The expression profiles of LINC00520 and SLC7A11 in various cancers were analyzed using the TCGA database. Using renal cell carcinoma cell lines, the interactions between LINC00520, miR-372, and SLC7A11 were validated through qRT-PCR, Western blot, RNA immunoprecipitation (RIP), and dual-luciferase reporter assays. The effects of LINC00520 on the cell cycle, apoptosis, migration, invasion, and proliferation of renal cancer cells were evaluated using techniques such as flow cytometry, Transwell assay, and immunofluorescence staining. The involvement of miR-372 was validated through functional rescue experiments. Result: LINC00520 and SLC7A11 showed high expression in various cancers (including ccRCC), and their expression levels in ccRCC were positively correlated with tumor staging and grading. Mechanistically, LINC00520 acts as a ceRNA by directly binding to miR-372, relieving its inhibition of the target gene SLC7A11 and upregulating its expression. Functionally, overexpression of LINC00520 can promote the cell cycle progression, migration, invasion, proliferation, and inhibit apoptosis of renal cancer cells, which can be partially reversed by miR-372 mimetics. On the contrary, knocking down LINC00520 produces the opposite phenotype, and this effect can be partially rescued by miR-372 inhibitors. In addition, LINC00520 can downregulate the expression of the tumor suppressor gene P53. LINC00520 plays a pro-cancer role in renal cell carcinoma by adsorbing miR-372 through ceRNA, thereby releasing the inhibition of SLC7A11 by miR-372 and ultimately promoting tumor malignant progression. The LINC00520/miR-372/SLC7A11 axis is a potential prognostic biomarker and therapeutic target for renal cell carcinoma.
Insights
Long non-coding RNA LINC00520 promotes clear cell renal cell carcinoma (ccRCC) by acting as a competitive endogenous RNA (ceRNA). It upregulates SLC7A11 by sponging miR-372, driving tumor progression and impacting cell cycle and apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Clear cell renal cell carcinoma (ccRCC) is a significant health concern with complex molecular underpinnings.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development and progression.
- Understanding the regulatory networks involving lncRNAs, microRNAs, and target genes is crucial for identifying novel therapeutic strategies.
Purpose of the Study:
- To elucidate the role of LINC00520 as a competitive endogenous RNA (ceRNA) in ccRCC.
- To investigate the regulatory mechanism of LINC00520 on the miR-372/SLC7A11 axis in ccRCC progression.
- To assess the potential of the LINC00520/miR-372/SLC7A11 axis as a prognostic biomarker and therapeutic target for ccRCC.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) database for expression profiles of LINC00520 and SLC7A11.
- Validation of molecular interactions using qRT-PCR, Western blot, RNA immunoprecipitation (RIP), and dual-luciferase reporter assays in ccRCC cell lines.
- Functional assays including flow cytometry, Transwell assays, and immunofluorescence staining to evaluate cellular processes; functional rescue experiments to confirm miR-372 involvement.
Main Results:
- LINC00520 and SLC7A11 exhibited high expression in ccRCC, correlating positively with tumor stage and grade.
- LINC00520 directly binds to miR-372, functioning as a ceRNA to upregulate SLC7A11 expression by relieving miR-372's inhibition.
- Overexpression of LINC00520 promoted ccRCC cell proliferation, migration, and invasion while inhibiting apoptosis, effects partially reversed by miR-372 mimics; knockdown yielded opposite results.
Conclusions:
- LINC00520 acts as an oncogenic lncRNA in ccRCC by sponging miR-372, leading to SLC7A11 upregulation and promoting tumor malignancy.
- The LINC00520/miR-372/SLC7A11 axis represents a promising therapeutic target and prognostic biomarker for ccRCC patients.
- LINC00520 also influences the tumor suppressor gene P53, further contributing to ccRCC progression.
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