MicroRNA-340-5p suppresses non-small cell lung cancer cell growth and metastasis by targeting ZNF503

Lu, Guojie; Zhang, Yaosen

doi:10.1186/s11658-019-0161-1

Cited by 34 publications

(22 citation statements)

References 26 publications

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“…Our evidences indicated that miR-340-5p acts as a tumor suppressor in glioma. Those data were in accordance with the previous reports that miR-340 functioned as a tumor suppressor in several cancers, including gastric cancer, breast cancer, squamous cell carcinoma, ovarian cancer, osteosarcoma, multiple myeloma and non-small cell lung cancer [44,45]. In this study, we found that the expressions of LINC00662, STAT3 and STAT3 target genes were downregulated with miR-340-5p OE in U251 cells.…”

Section: Discussionsupporting

confidence: 93%

The Function of LINC00662/miR-340-5p/STAT3 Regulation Loop in Promoting Tumorigenesis and Development of Glioma

Song

Cheng

et al. 2020

Preprint

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Background: Long noncoding RNAs( lncRNAs) have been reported to be associated with tumorigenesis and development of glioma. LINC00662 has been implicated in pathogenesis of various human cancers. However, role of LINC00662 in glioma remains unknown.Methods: Bioinformatics methods were used to analysis the expression of LINC00662 in glioma. RT-qPCR was performed to examine the expression levels of LINC00662 in glioma tissues and cell lines. The effect of LINC00662 in cell proliferation and invasion was evaluated by Cell Counting Kit-8(CCK-8), clone colony formation and transwell assay. Luciferase reporter assays were performed to investigate the interaction between miR-340-5p and LINC00662, 3’UTR of STAT3. CHIP-qPCR and Luciferase reporter assays were used to demonstrate the interaction between STAT3 and the promoter region of LINC00662. Rescue assays and Tumor xenografts in nude mice were applied to verify the effect of LINC00662 in modulating miR-340-5p/ STAT3 signal pathway.Results: LINC00662 was frequently high expressed and associated with malignant phenotype of glioma. LINC00662 knockdown inhibited proliferation, invasion and glioma-genesis of glioma. Moreover, LINC00662 knockdown repressed development of glioma by inhibiting the expression and activation of STAT3 pathway. Mechanically, LINC00662 acted as a ceRNA sponging miR-340-5p to protect the expression of STAT3. More importantly, LINC00662 was one of direct target genes of STAT3.Conclusions: There was a positive regulation loop between LINC00662 and STAT3. LINC00662 might be an oncogene in glioma. Targeting LINC00662 was a potential strategy in glioma therapy.

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Section: Discussionsupporting

confidence: 93%

The Function of LINC00662/miR-340-5p/STAT3 Regulation Loop in Promoting Tumorigenesis and Development of Glioma

Song

Cheng

et al. 2020

Preprint

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“…31 Recent evidence suggested that miR-340-5p hindered non-small cell lung cancer progression through degradation of ZNF503. 32 In the current study, ZNF503 was distinctly up-regulated in NSCLC. More importantly, ZNF503 overexpression reversed the inhibitory effect of TTN-AS1 depletion on NSCLC progression.…”

Section: Dovepresssupporting

confidence: 48%

<p>LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis</p>

2020

OTT

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Background: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high mortality worldwide. Long non-coding RNA (lncRNA) TTN antisense RNA1 (TTN-AS1) has been demonstrated to play a crucial role in a variety of cancers. This study was designed to investigate the function and molecular mechanism of lncRNA TTN-AS1 in NSCLC. Methods: The expression levels of TTN-AS1, miR-491-5p and zinc finger protein 503 (ZNF503) were examined by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assay, respectively. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell migration and invasion were assessed by transwell assay. Epithelial-to-mesenchymal transition (EMT)-related proteins were measured using Western blot assay. The relationship between TTN-AS1, miR-491-5p and ZNF503 was predicted by starBase2.0 and confirmed by dual-luciferase reporter assay. Xenograft tumor experiment was conducted to analyze the tumor growth in vivo. Results: The levels of TTN-AS1 and ZNF503 were up-regulated, while miR-491-5p expression was reduced in NSCLC tissues and cells. Knockdown of TTN-AS1 or ZNF503 suppressed cell proliferation, migration, invasion and EMT in NSCLC cells. Overexpression of ZNF503 reversed the effect of TTN-AS1 silencing on NSCLC progression. TTN-AS1 could modulate the expression of ZNF503 via sponging miR-491-5p. Furthermore, TTN-AS1 induced tumor growth in vivo. Conclusion: Inhibition of TTN-AS1 hindered cell proliferation, migration, invasion and EMT in NSCLC cells by modulating miR-491-5p/ZNF503 axis, providing a promising biomarker for NSCLC treatment.

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“… Zhou and Li demonstrated that miR‐605 restoration hindered the metastasis of NSCLC . Upregulation of miR‐340 repressed tumor growth and metastasis of NSCLC in the study by Lu and Zhang . Similarly, miR‐150 exhibited an inhibitory effect on the metastasis of NSCLC .…”

Section: Discussionmentioning

confidence: 98%

MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

et al. 2019

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Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. MiRNAs are recognized as important molecules in cancer biology. The aim of the study was to identify a novel biomarker miR-148b and its mechanism in the modulation of NSCLC progression. Methods: The expressional level of miR-148b was analyzed by RT-PCR. The effect of miR-4317 on proliferation was evaluated through 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2Htetrazolium bromide (MTT) assay. The effect of miR-148b on the metastasis of NSCLC was detected through transwell assays. The verification of the target of miR-148b was assessed by TargetScan and dualluciferase reporter assay. The related proteins in this study were analyzed by western blot. Results: Our findings confirmed that miR-148b was decreased in NSCLC and NSCLC patients with lower expression exhibited poorer overall survival (OS). Increasing miR-148b significantly repressed proliferation, invasion and migration. More importantly, activated leukocyte cell adhesion molecule (ALCAM) was determined as the direct target of miR-148b, and reintroduction of ALCAM attenuated miR-148b effect on the progress of NSCLC. In addition, NF-κB signaling pathway was modulated by miR-148b/ALCAM axis. Conclusions: Our results indicated that miR-148b is able to suppress NSCLC growth and metastasis via targeting ALCAM through the NF-κB pathway. These findings provided new evidence that miR-148b serves as a potential biomarker and novel target for NSCLC treatment.

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MicroRNA-340-5p suppresses non-small cell lung cancer cell growth and metastasis by targeting ZNF503

Cited by 34 publications

References 26 publications

The Function of LINC00662/miR-340-5p/STAT3 Regulation Loop in Promoting Tumorigenesis and Development of Glioma

The Function of LINC00662/miR-340-5p/STAT3 Regulation Loop in Promoting Tumorigenesis and Development of Glioma

<p>LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis</p>

MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

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