Dataset Information

Blocking circ_0000520 Suppressed Breast Cancer Cell Growth, Migration and Invasion Partially via miR-1296/SP1 Axis Both in vitro and in vivo.

ABSTRACT: Background:Breast cancer (BCa) is an overwhelming malignant tumor mainly in women globally. Circular RNAs (circRNAs) are a special type of noncoding RNAs involved in competing endogenous RNA (ceRNA) network, a classic molecular mechanism of the tumorigenesis of human cancers, including BCa. Here, we intended to explore the role and mechanism of hsa_circ_0000520 (circ_0000520) in BCa cells. Methods:Expression of circ_0000520, miRNA-1296-5p (miR-1296) and specificity protein 1 (SP1) was measured by real time-quantitative PCR and Western blotting. Cell growth was measured by cell counting kit-8, colony formation assay and flow cytometry method. Cell migration and invasion were assessed by transwell assays and Western blotting. Tumor growth was determined by xenograft models. The direct interaction among circ_0000520, miR-1296 and SP1 was confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results:circ_0000520 was upregulated in BCa tumors and cell lines (T47D, MCF7, MDA-MB-231, BT549, and SKBR3), and circ_0000520 high expression was associated with poor overall survival. Blocking circ_0000520 suppressed cell viability, colony formation, migration and invasion, but promoted cell cycle arrest and apoptosis rate in MDA-MB-231 and MCF7 cells. circ_0000520 could directly regulate miR-1296 expression, and SP1 was a novel target for miR-1296. Moreover, the anti-tumor role of circ_0000520 silencing was abrogated by miR-1296 downregulation or SP1 restoration. Notably, tumor growth of MDA-MB-231 cells in mice was restrained by circ_0000520 deletion. Conclusion:circ_0000520 knockdown could suppress cell growth, migration and invasion both in vitro and in vivo through regulating miR-1296/SP1 pathway.

SUBMITTER: Zang H

PROVIDER: S-EPMC7457856 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Blocking circ_0000520 Suppressed Breast Cancer Cell Growth, Migration and Invasion Partially via miR-1296/SP1 Axis Both in vitro and in vivo.

Zang Hongliang H Li Yuhui Y Zhang Xue X Huang Guomin G

Cancer management and research 20200825

<h4>Background</h4>Breast cancer (BCa) is an overwhelming malignant tumor mainly in women globally. Circular RNAs (circRNAs) are a special type of noncoding RNAs involved in competing endogenous RNA (ceRNA) network, a classic molecular mechanism of the tumorigenesis of human cancers, including BCa. Here, we intended to explore the role and mechanism of <i>hsa_circ_0000520</i> (<i>circ_0000520</i>) in BCa cells.<h4>Methods</h4>Expression of <i>circ_0000520</i>, <i>miRNA-1296-5p</i> (<i>miR-1296</ ...[more]

PMID: 32922078

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Project description:Long non-coding RNA tissue differentiation-inducing non-protein coding (TINCR) is associated with the carcinogenesis of several cancers. However, little is known about the function and mechanism of TINCR in lung adenocarcinoma (LUAD). Here, we aimed to analyze expression of TINCR and elucidate its mechanistic involvement in the progression of LUAD. The expression of TINCR was investigated according to Gene Expression Profiling Interactive Analysis at first and then detected in 29 LUAD tissues and paired adjacent normal tissues using qRT-PCR. Results indicated that TINCR was evidently downregulated in LUAD. The association between TINCR and clinicopathological parameters was analyzed by Pearson's chi-square test, suggesting TINCR was closely correlated with TNM stage and lymph mode metastasis. Subsequently, the function role of TINCR was examined by gain- and loss-of-function studies in LUAD (A549 and NCI-H292) cells. As analyzed by the scratch wound-healing and transwell assays, results revealed that TINCR suppressed the migration and invasion of A549 and NCI-H292 cells. However, TINCR exerted no effects on the cell proliferation as determined by CCK8 assay. Furthermore, we reported that loss of Sp1 could inhibit TINCR expression. Expressions of miR-107/miR-1286 were detected by qRT-PCR assay in A549 and NCI-H292 cells after TINCR knockdown or overexpression. In addition, the direct binding ability of the predicted miR-107 or miR-1286 binding site on TINCR was validated by luciferase activity assay. Results indicated TINCR could constrain the expression of miR-107/miR-1286, and was a target of them in LUAD cells. Bioinformatics analyses showed that BTRC and RAB14 was the potential target gene of miR-107 and miR-1286, respectively. These data revealed a possible regulatory mechanism in which upregulation of TINCR induced by Sp1 could constrain the migration and invasion through regulating miR-107 or miR-1286 in LUAD cells. Conjointly, our findings provide a valuable insight into the regulatory mechanism of TINCR in LUAD, supportive to its potential of therapeutic target for LUAD patients.

Dataset Information

Blocking circ_0000520 Suppressed Breast Cancer Cell Growth, Migration and Invasion Partially via miR-1296/SP1 Axis Both in vitro and in vivo.

Publications

Blocking circ_0000520 Suppressed Breast Cancer Cell Growth, Migration and Invasion Partially via miR-1296/SP1 Axis Both in vitro and in vivo.

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