LINC‐PINT alleviates lung cancer progression via sponging miR‐543 and inducing PTEN

Wang, Shu; Jiang, Wenyang; Zhang, Xinghua; Lu, Zilong; Geng, Qing; Wang, Wei; Li, Nan; Cai, Xinyong

doi:10.1002/cam4.2822

Cited by 33 publications

(27 citation statements)

References 31 publications

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“…13 For example, LINC-PINT weakens the growth and colony formation of A549 and H1299, and inhibits the migration and invasion of NSCLC cells by regulating different genes. 14,15 On the other side, studies have also suggested that lncRNAs aggravate NSCLC progression. For instance, Ye et al found that lncRNA-BLACAT1 accelerates the growth, migration and metastasis of NSCLC by sponging miR-144.…”

Section: Discussionmentioning

confidence: 99%

LINC00680 Promotes the Progression of Non-Small Cell Lung Cancer and Functions as a Sponge of miR-410-3p to Enhance HMGB1 Expression

Wang

Li²,

Zheng³

et al. 2020

OTT

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Purpose: LINC00680 was reported to be involved in various cancers through multiple mechanisms. Therefore, we intended to investigate its role in the progression of non-small cell lung cancer (NSCLC). Materials and Methods: Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was used to test LINC00680 in NSCLC tissue and cell lines. Subsequently, A549 and H1299 cells were transfected with LINC00680 overexpressing plasmids and their proliferation and colony formation and apoptosis was tested by Transwell assay and flow cytometry. In addition, xenograft tumor experiments in nude mice also affirmed. Meanwhile, we predicted that miR-410-3p, LINC00680 and high-mobility group protein box 1(HMGB1) relationship by Starbase, dual-luciferase reporter and RIP assay. Finally, the carcinogenic effects of LINC00680 were reversed by ethyl pyruvate (EP), a specific inhibitor of HMGB1. Results: LINC00680 was upregulated in NSCLC and was closely related to the malignancy and poor prognosis of NSCLC patients. LINC00680 promoted proliferation and colony formation and inhibited apoptosis of A549 and H1299 cells. In addition, overexpressing LINC00680 accelerated the growth of NSCLC cells in xenograft tumor experiments in nude mice also affirmed. Meanwhile, high-mobility group protein box 1(HMGB1) was astoundingly amplified in NSCLC and was negatively regulated by miR-410-3p. Further, HMGB1 acted as a downstream target of miR-410-3p, upregulating miR-410-3p to attenuate HMGB1, while LINC00680 strengthened the expression of HMGB1 in A549 and H1299 cells. Discussion: Thus, these results indicated that LINC00680 was cancerogenic in NSCLC by upregulating HMGB1 via sponging miR-410-3p.

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Section: Discussionmentioning

confidence: 99%

LINC00680 Promotes the Progression of Non-Small Cell Lung Cancer and Functions as a Sponge of miR-410-3p to Enhance HMGB1 Expression

Wang

Li²,

Zheng³

et al. 2020

OTT

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“…18 LINC-PINT inhibits lung cancer cell growth, cell cycle, migration and invasion while promoting apoptosis. 19 In addition, lncRNA MIAT upregulation leads to accelerated cell growth and predicts poor prognosis in lung cancer. 14 There are still a lot of lncRNAs whose functions are unclear in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA PSMA3-AS1 Promotes Lung Cancer Growth and Invasion via Sponging MiR-4504

Zhu

2020

CMAR

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Background: Long noncoding RNAs (lncRNAs) have close correlation with tumorigenesis. And how lncRNAs participate in lung cancer require investigation in-depth. The aim of this study was to determine the role of lncRNA PSMA3-AS1 in lung cancer progression. Methods: PSMA3-AS1 expression was analyzed via qRT-PCR. Kaplan-Meier method was used to analyze survival rate based on PSMA3-AS1 value. Proliferation was measured via CCK8 and colony formation assays. Transwell assay was utilized to examine migration and invasion. Luciferase reporter assay and RNA pulldown assay were utilized to analyze the interaction between PSMA3-AS1 and miR-4504. Results: PSMA3-AS1 expression was upregulated in lung cancer tissues and cell lines. PSMA3-AS1 expression was positively correlated with clinical stage and metastasis. PSMA3-AS1 overexpression predicted a poor prognosis in lung cancer patients. PSMA3-AS1 knockdown suppressed proliferation, migration and invasion of lung cancer cells. Through bioinformatics analysis, PSMA3-AS1 was predicted to sponge miR-4504. MiR-4504 expression was inhibited by PSMA3-AS1. And inhibition of miR-4504 reversed the effects of PSMA3-AS1 depletion. Conclusion: PSMA3-AS1 promotes the tumorigenesis of lung cancer through inhibiting miR-4504.

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“…In addition, qRT-PCR results displayed that miR-543 expression in NSCLC tissues and their cell lines was significantly up-regulated ( Figure 3D and E), which was consistent with previous report. 16 In addition, it was observed that GATA6-AS1 overexpression could down-regulate miR-543 expression in H1299 cells, while knocking down GATA6-AS1 could lead to opposite result in H460 cells ( Figure 3F). These results suggested that GATA6-AS1 targeted miR-543 to negatively regulate its expression.…”

Section: Gata6-as1 Targeted Mir-543mentioning

confidence: 90%

“…15 A previous study reports that miR-543 is highly expressed in NSCLC and exerts tumor-promoting effects via repressing PTEN. 16 However, the mechanism of abnormal expression of miR-543 in NSCLC is not clear.…”

Section: Introductionmentioning

confidence: 99%

LncRNA GATA6-AS1 Inhibits the Progression of Non-Small Cell Lung Cancer via Repressing microRNA-543 to Up-Regulating RKIP

Gong¹,

Chen

Zhang

et al. 2020

CMAR

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Background: Much evidence unveils the significance of long non-coding RNAs (lncRNAs) in diverse cancers. This study was designed to clarify the function and mechanism of lncRNA GATA6 antisense RNA 1 (GATA6-AS1) in the progression of non-small cell lung cancer (NSCLC). Methods: GATA6-AS1, miR-543 and Raf kinase inhibitor protein (RKIP) mRNA expressions were detected by qRT-PCR. Chi-square test was adopted to analyze the relationship between GATA6-AS1 expression and the clinicopathological parameters of NSCLC patients. NSCLC cells H1299 and H460 cells were used as overexpression or knockdown models, respectively, and cell proliferation and metastasis were determined by CCK-8 and Transwell assays. RKIP, E-cadherin, N-cadherin, STAT3, p-STAT3 expressions in NSCLC cells were detected by Western blot. The targeting relationship between GATA6-AS1 and miR-543 was confirmed by dual-luciferase reporter assay. Results: GATA6-AS1 was significantly lowly expressed in NSCLC tissues and cell lines, and its low expression level was significantly correlated with larger tumor size and positive lymph node metastasis. GATA6-AS1 overexpression inhibited the proliferation, migration, invasion and epithelial-mesenchymal transition of NSCLC cells, while GATA6-AS1 knockdown caused the opposite effects. Mechanistically, it was confirmed that GATA6-AS1 impeded NSCLC cell proliferation and metastasis by adsorbing miR-543 and up-regulating the expression of RKIP. Conclusions: As a tumor suppressor, GATA6-AS1 participates in suppressing the progression of NSCLC by modulating the miR-543/RKIP axis.

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LINC‐PINT alleviates lung cancer progression via sponging miR‐543 and inducing PTEN

Cited by 33 publications

References 31 publications

<p>LINC00680 Promotes the Progression of Non-Small Cell Lung Cancer and Functions as a Sponge of miR-410-3p to Enhance HMGB1 Expression</p>

<p>LINC00680 Promotes the Progression of Non-Small Cell Lung Cancer and Functions as a Sponge of miR-410-3p to Enhance HMGB1 Expression</p>

<p>LncRNA PSMA3-AS1 Promotes Lung Cancer Growth and Invasion via Sponging MiR-4504</p>

<p>LncRNA GATA6-AS1 Inhibits the Progression of Non-Small Cell Lung Cancer via Repressing microRNA-543 to Up-Regulating RKIP</p>

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