TGF-β/SMAD4-Regulated LncRNA-LINP1 Inhibits Epithelial-Mesenchymal Transition in Lung Cancer

Zhang, Chong; Hao, Yajing; Wang, Yanxiao; Xu, Jiaqian; Teng, Yan; Yang, Xiao

doi:10.7150/ijbs.27197

Cited by 47 publications

(37 citation statements)

References 22 publications

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“…lncRNAs have been reported as potential prognostic biomarkers and important regulatory factors of many types of cancer, 25,26 including liver cancer, 27 BC, 28 and lung cancer 29 . It is evident that lncRNA has the ability to act as miRNA sponges, which functioned as endogenous miRNA sponges via binding with miRNA 30 .…”

Section: Discussionmentioning

confidence: 99%

lncRNA CERS6‐AS1 as ceRNA promote cell proliferation of breast cancer by sponging miR‐125a‐5p to upregulate BAP1 expression

Yan

Feng

et al. 2020

Molecular Carcinogenesis

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Long noncoding RNAs (lncRNAs) can act as oncogene and tumor suppressor genes in many types of cancers including breast cancer (BC). Our previous study has indicated microRNA (miR)‐125a‐5p was downregulated and function as a tumor suppressor in BC. However, its upstream regulation mechanism is still unclear. In this study, we used bioinformatics algorithms, RNA pulldown assay, and dual‐luciferase reports assay to predict and confirm lncRNA CERS6‐AS1 interacted with miR‐125a‐5p. Then we found CERS6‐AS1 was upregulated in BC tissues. Experimental results of tumor growth in nude mice show that CERS6‐AS1 promotes tumor growth. Furthermore, CERS6‐AS1 regulated BC susceptibility gene 1‐associated protein 1 (BAP1) expression via sponging miR‐125a‐5p via Western blot analysis and quantitative polymerase chain reaction arrays. Finally, we showed that miR‐125a‐5p had opposing effects to those of CERS6‐AS1 on BC cells, demonstrating that CERS6‐AS1 may promote cell proliferation and inhibit cell apoptosis via sponging miR‐125a‐5p. Our results indicated CERS6‐AS1 promote BC cell proliferation and inhibit cell apoptosis via sponging miR‐125a‐5p to upregulate BAP1 expression.

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Section: Discussionmentioning

confidence: 99%

lncRNA CERS6‐AS1 as ceRNA promote cell proliferation of breast cancer by sponging miR‐125a‐5p to upregulate BAP1 expression

Yan

Feng

et al. 2020

Molecular Carcinogenesis

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“…Many of these lncRNAs are regulated by TGF-β. [11][12][13][14][15] LncRNAs play essential roles in the migration, invasion and EMT and are discovered to act as miRNA sponges to participate in cancer progression. [16][17][18] Our previous study has shown that six lncRNAs, including LINC02323, are associated with metastasis and prognosis of LUAD.…”

Section: Introductionmentioning

confidence: 99%

Novel long non‐coding RNA LINC02323 promotes epithelial‐mesenchymal transition and metastasis via sponging miR‐1343‐3p in lung adenocarcinoma

Zhang

Han

et al. 2020

Thoracic Cancer

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Background We have previously developed a unique metastasis‐associated signature consisting of six long non‐coding RNAs (lncRNAs), including a novel lncRNA, namely LINC02323. In the present study, we aimed to investigate the underlying roles of LINC02323 in the migration, invasion and TGF‐β‐induced epithelial‐mesenchymal transition (EMT) of lung adenocarcinoma (LUAD) cells. Methods The distribution of LINC02323 was detected by the nuclear‐plasma separation experiment. Cell proliferation was assessd by MTT assay, and cell migration and invation were detected by transwell assays. EMT was detected by RT‐qPCR and western blotting. Interaction between miRNA and LINC02323 was predicted by starBase v2.0 and confirmed by the double luciferase reporting system. Results LINC02323 was distributed in the cytoplasm and nucleus. The overexpression or deletion of LINC02323 did not affect the proliferation of LUAD cells, while significantly affected the migration and invasion of LUAD cells. TGF‐β‐induced EMT process was significantly affected by both RNA interference (RNAi) and overexpression of LINC02323. The predicted results showed that there were binding sites between LINC02323 and miR‐1343‐3p. The expression of LINC02323 was found to be negatively correlated with miR‐1343‐3p in LUAD by analyzing The Cancer Genome Atlas (TCGA) database. The double luciferase reporting system, RT‐qPCR and western blotting experiments confirmed that LINC02323 could bind to miR‐1343‐3p, which bound to TGF‐β receptor 1 (TGFBR1). Inhibition of miR‐1343‐3p reversed LINC02323 silencing‐mediated suppression of migration, invasion and EMT. Conclusions LINC02323 acts as a competing endogenous RNA (ceRNA), which sponged miR‐1343‐3p to upregulate the TGFBR1 expression and promote the EMT and metastasis in LUAD. Key points Significant findings of the study LINC02323 promotes epithelial‐mesenchymal transition and metastasis via sponging miR‐1343‐3p in lung adenocarcinoma. What this study adds LINC02323 is a key molecule in the process of invasion and metastasis of LUAD and might be used as a potential target in metastatic cancer.

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“…Growing evidence has demonstrated that TGF-β-related lncRNAs play pivotal roles in the progression of tumorigenesis through regulating EMT. 36,37 During the process of EMT, epithelial markers (such as E-cadherin) are downregulated and mesenchymal markers (such as N-cadherin and vimentin) are upregulated. 38,39 In the present study, we confirmed that the expression of LOC440173 was associated with cell migration and invasion and that LOC440173 was upregulated in TGF-β-treated Eca109 cells.…”

Section: Discussionmentioning

confidence: 99%

A novel long noncoding RNA, LOC440173, promotes the progression of esophageal squamous cell carcinoma by modulating the miR‐30d‐5p/HDAC9 axis and the epithelial–mesenchymal transition

Wang

Feng

Niu

et al. 2020

Molecular Carcinogenesis

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Countless evidence suggests that long noncoding RNAs (lncRNAs) are involved in human malignant cancers, including esophageal squamous cell carcinoma (ESCC), although their exact function remains unclear. In the present study, we aimed to investigate the roles and molecular mechanisms of the lncRNA LOC440173 in ESCC progression. Microarray analysis and quantitative real-time polymerase chain reaction were conducted to measure the expression levels of LOC440173 and miR-30d-5p. The biological function of this lncRNA was investigated using the 3-(4,5dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, clone formation, and transwell assays, as well as flow cytometry and Western blot analysis. The function of LOC440173 was validated in vivo using tumor xenografts. The regulatory network of LOC440173/miR-30d-5p/HDAC9 was established using bioinformatic analysis and verified with dual-luciferase reporter assays, RNA immunoprecipitation assay, and rescue experiments. The expression level of LOC440173 was significantly increased in ESCC tissues and esophageal carcinoma cells. High LOC440173 expression was correlated with histological grade, tumor invasion depth, lymph node metastasis, and TNM stage. Overexpression of LOC440173 promoted esophageal cancer cell proliferation, migration, and invasion, as well as the epithelial-mesenchymal transition (EMT) process in vitro, and facilitated tumor growth in vivo. MicroRNA-30d-5p (miR-30d-5p) was downregulated in ESCC tissues and acted as a direct binding target of LOC440173 during the regulation of HDAC9 expression in esophageal carcinoma cells. In conclusion, LOC440173 exerts a promotive role in ESCC tumorigenesis by targeting the miR-30d-5p/HDAC9 axis and

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TGF-β/SMAD4-Regulated LncRNA-LINP1 Inhibits Epithelial-Mesenchymal Transition in Lung Cancer

Cited by 47 publications

References 22 publications

lncRNA CERS6‐AS1 as ceRNA promote cell proliferation of breast cancer by sponging miR‐125a‐5p to upregulate BAP1 expression

lncRNA CERS6‐AS1 as ceRNA promote cell proliferation of breast cancer by sponging miR‐125a‐5p to upregulate BAP1 expression

Novel long non‐coding RNA LINC02323 promotes epithelial‐mesenchymal transition and metastasis via sponging miR‐1343‐3p in lung adenocarcinoma

A novel long noncoding RNA, LOC440173, promotes the progression of esophageal squamous cell carcinoma by modulating the miR‐30d‐5p/HDAC9 axis and the epithelial–mesenchymal transition

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