LINC00461 promotes cell migration and invasion in breast cancer through miR‐30a‐5p/integrin β3 axis

Dong, Lifeng; Qian, Junbin; Chen, Fangfang; Fan, Yangfan; Long, Jingpei

doi:10.1002/jcb.27435

Cited by 43 publications

(39 citation statements)

References 40 publications

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“…After 60-min blocking at 25°C using 5% BSA, the membranes were incubated at 4°C with the indicated primary antibody overnight. The primary antibody against: RAP2A (ab49685, Abcam, 1:1000), AKT (ab8805, Abcam, 1:1000) [45], phosphor AKT (ab38449, Abcam, 1:1000) [46], and GAPDH (ab8245, Abcam, 1:2500) were used. Subsequently, a 60 min of incubation of the membranes at 25°C was done with the goat anti-rabbit/mouse IgG secondary antibodies, as appropriate.…”

Section: Western Blotting (Wb)mentioning

confidence: 99%

RETRACTED ARTICLE: MiR-140 targets RAP2A to enable the proliferation of insulin-treated ovarian granulosa cells

Xiong

Wang

et al. 2020

J Ovarian Res

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Background: We elucidated the role of specific MicroRNAs (miRNAs) in the development of polycystic ovary syndrome (PCOS) and explained the changes in the proliferation of granulosa cells. Excised ovarian cortex specimens were collected for miRNA profiling analysis (n = 20 PCOS females and 5 non-PCOS females). Insulintreated ovarian granulosa cells isolated from mice were used for mechanical studies. Results: High miR-140 expression was observed in PCOS samples and insulin-treated granulosa cells compared to that in non-PCOS and unstimulated cells, respectively. However, the Ras-related protein Rap-2a precursor (RAP2A) was downregulated in in PCOS. MTT assay and EdU staining showed that an miR-140 inhibitor attenuated viability in insulin-treated granulosa cells; cell viability increased with miR-140 overexpression. Reduced expression of miR-140 and the expression of the miR-140 mimic resulted in marked cell apoptosis, as evidenced by the results of PI flow cytometry and Annexin V-FITC; miR-140 overexpression results in downregulated RAP2A expression, and the miR-140 mimic directly bound to the RAP2A 3′-UTR, causing increase in RAP2A levels in insulin-treated granulosa cells; RNA-mediated silencing of RAP2A in insulin-treated granulosa cells restored cell proliferation and apoptosis to normal levels. Phosphorylated AKT was found to be negatively regulated through cross-talk between miR-140 and RAP2A. Conclusions: In conclusion, PCOS ovarian cortex specimens and insulin-treated granulosa cells showed elevated expression of miR-140, which could lead to increased proliferation and reduced apoptosis of cells by targeting RAP2A. This study may pave the way for future research on the properties of granulosa cells in PCOS.

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Section: Western Blotting (Wb)mentioning

confidence: 99%

RETRACTED ARTICLE: MiR-140 targets RAP2A to enable the proliferation of insulin-treated ovarian granulosa cells

Xiong

Wang

et al. 2020

J Ovarian Res

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“…Mounting studies have suggested the significant role of lncRNAs in the development of cancers, including NSCLC [14][15][16]. Herein, we selected LINC00461 for investigation because it has been demonstrated as an oncogene in multiple cancers, such as breast cancer, myeloma, and glioma [17][18][19]. In the present study, we firstly found that LINC00461 was up-regulated in NSCLC, and indicated poor prognosis.…”

Section: Discussionmentioning

confidence: 65%

“…The effect of lncRNAs on NSCLC has also been uncovered by mounting researches [14][15][16]. Long intergenic non-protein coding RNA 461 (LINC00461) demonstrated oncogenic performance in breast cancer, myeloma, and glioma [17][18][19], promoting cell growth, migration, and invasion, but it is not researched in NSCLC.…”

Section: Introductionmentioning

confidence: 99%

LINC00461/miR-4478/E2F1 feedback loop promotes non-small cell lung cancer cell proliferation and migration

2020

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Non-small cell lung cancer (NSCLC) is a prevalent subtype of lung cancer, whose mortality is high. Long non-coding RNAs (lncRNAs) have caught rising attentions because of their intricate roles in regulating cancerization and cancer progression. Long intergenic non-protein coding RNA 461 (LINC00461) has recently shown oncogenic potential in several cancers, but the function of LINC00461 in NSCLC remains to be investigated. Our study planned to unveil the regulatory role of LINC00461 in NSCLC. It was validated that LINC00461 was highly expressed in NSCLC tissues and cell lines and exhibited prognostic significance. Furthermore, LINC00461 expression in advanced stage was much higher than in early stage. Loss-of-function experiments suggested that LINC00461 knockdown impaired cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT). Subcellular fractionation revealed the predominant location of LINC00461 in cytoplasm. Mechanistically, LINC00461 up-regulated E2F transcription factor 1 (E2F1) expression through sponging miR-4478. Besides, E2F1 bound to the promoter of LINC00461 to induce its transcription. Finally, rescue experiments verified that LINC00461 aggravated proliferation, migration, and EMT through targeting miR-4478/E2F1 axis. In consequence, the present study illustrated that LINC00461/miR-4478/E2F1 feedback loop promoted NSCLC cell proliferation and migration, providing a new prognostic marker for NSCLC.

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“…In the present study, we downloaded the data of gene and miRNA expression quantification from the TCGA-BRCA dataset, and identified DEGs, DElncR-NAs and DEmiRNAs, finding that LINC00461 exhibited a much higher expression in breast cancer. Given that LINC00416 has been reported to be able to promote cell invasion and migration in breast cancer [11], we made some further steps for validation. In addition, it has been revealed that LINC00461 can mediate cell invasion and migration in hepatocellular carcinoma via serving as a ceRNA that can competitively bind to miR-149-5p [10].…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have described that LINC00461 is a vital player in glioma progression responsible for mediating cell proliferation, invasion and migration via MAPK/ERK, PI3K/AKT and other possible signaling pathways [9], and it can be involved in the LINC00461/miR-149-5p/LRIG2 axis in turn participating in the progression of hepatocellular carcinoma [10]. However, the role of LINC00461 in breast cancer is poorly reported [11].…”

Section: Introductionmentioning

confidence: 99%

A long non-coding RNA LINC00461-dependent mechanism underlying breast cancer invasion and migration via the miR-144-3p/KPNA2 axis

et al. 2020

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Background: The purpose of this study was to explore the regulatory mechanism of the long non-coding RNA (lncRNA) LINC00461 underlying the breast cancer invasion and migration via the miR-144-3p/KPNA2 axis. Methods: Bioinformatics methods were applied to screen differentially expressed mRNAs, miRNAs and lncRNAs for construction of a competing endogenous RNA (ceRNA) network. LINC00461, KPNA2 and miR-144-3p were identified, and KPNA2 was predicted to be a target of miR-144-3p and significantly correlated with breast cancer prognosis. To make the findings more convincible, we used qRT-PCR to detect the expression levels of LINC00461 and miR-144-3p in breast cancer cells, and conducted western blot to determine KPNA2 protein level. Then, RIP was performed to assess the combination between miR-144-3p and LINC00461 or KPNA2, and dual-luciferase reporter assay was used to validate the targeted relationship between miR-144-3p and KPNA2. Furthermore, Transwell was employed for the examination of cell invasion and migration in breast cancer. Results: LINC00461 was predicted to regulate KPNA2 through sponging miR-144-3p as revealed by the ceRNA network. Besides, LINC00461 and KPNA2 were found to be remarkably highly-expressed in breast cancer cells, while miR-144-3p was poorly-expressed. Silencing LINC00461 could promote miR-144-3p expression, thus inhibiting cell invasion and migration. In addition, KPNA2 was confirmed to be a direct target of miR-144-3p. Silencing miR-144-3p or overexpressing KPNA2 could reverse the inhibitory effect of LINC00461 silencing on cell invasion and migration in breast cancer. Conclusion: LINC00461 promoted the expression of KPNA2 by competitively binding to miR-144-3p, thereby promoting the invasion and migration of breast cancer cells.

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LINC00461 promotes cell migration and invasion in breast cancer through miR‐30a‐5p/integrin β3 axis

Cited by 43 publications

References 40 publications

RETRACTED ARTICLE: MiR-140 targets RAP2A to enable the proliferation of insulin-treated ovarian granulosa cells

RETRACTED ARTICLE: MiR-140 targets RAP2A to enable the proliferation of insulin-treated ovarian granulosa cells

LINC00461/miR-4478/E2F1 feedback loop promotes non-small cell lung cancer cell proliferation and migration

A long non-coding RNA LINC00461-dependent mechanism underlying breast cancer invasion and migration via the miR-144-3p/KPNA2 axis

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