Circular RNA circ_0067741 regulates the Hippo/YAP pathway to suppress lung adenocarcinoma progression by targeting microRNA-183-5p

Mo, Jianming; Nie, Hao; Zeng, Chao; Han, Hui; Xu, Ping; Shi, Xiaoshun

doi:10.1080/21655979.2022.2060901

Cited by 6 publications

(2 citation statements)

References 28 publications

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“…However, a newly published study reported plasma miR-183-5p in CRC patients with lymph node metastasis was abnormally overexpressed ( 38 ). More importantly, Mo et al ( 39 ) found miR-183-5p plays an oncogenic role in lung adenocarcinoma by targeting LATS1 and inhibiting the Hippo/YAP pathway . When taken together, these findings suggest the multiple pathogenic roles of miR-183-5p in various human cancer types and its use in tumor staging might be closely linked with its specific binding to different target genes.…”

Section: Discussionmentioning

confidence: 99%

miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4

Chen¹,

Zhou²,

Liao³

et al. 2023

J Thorac Dis

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Background Non-small cell lung cancer (NSCLC) progression is mediated by changes in gene expression induced by microRNAs. However, the underlying mechanisms remain to be elucidated. In this study, we investigated the roles of miR-183-5p and its target gene in lung cancer development. Methods Relative levels of miR-183-5p and lysyl oxidase-like 4 (LOXL4) expression in lung cancer cells or tissues were measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence or Western blotting as appropriate. The binding of miR-183-5p to LOXL4 sequences was verified by a dual luciferase reporter assay, and cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) and Edu staining. The cell cycle stage and apoptosis were detected by flow cytometry, and Transwell assays were performed to evaluate cell migration and invasion capabilities. The tumorigenic capability of cancer cells was analyzed using a cancer cell line-based xenograft nude mouse model. Results miR-183-5p expression was decreased in the lung cancer tissues and cell lines and was negatively correlated with elevated LOXL4 expression. Treatment with miR-183-5p mimics suppressed LOXL4 expression, while treatment with an miR-183-5p inhibitor promoted LOXL4 expression in A549 cells. miR-183-5p was found to directly bind to the 3’ UTR of the LOXL4 gene in A549 cells. Overexpression of LOXL4 enhanced cell proliferation, cell cycle progression, migration, and invasion, but repressed their apoptosis, and activated extracellular matrix (ECM) and the epithelial mesenchymal transition (EMT) process in A549 cells, while LOXL4 knockdown produced the opposite effects. Treatment with an miR-183-5P inhibitor promoted the proliferation, cell cycle progression, migration, and invasion of A549 cells but suppressed their apoptosis, and activated the ECM and EMT process, while all these effects were abrogated by LOXL4 knockdown. The tumorigenic capability of A540 cells in nude mice was greatly impaired by treatment with miR-183-5p mimics. Conclusions miR-183-5p repressed the proliferation, migration, invasion, ECM formation, and EMT processes, and promoted the apoptosis of lung cancer cells by targeting LOXL4 expression.

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Section: Discussionmentioning

confidence: 99%

miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4

Chen¹,

Zhou²,

Liao³

et al. 2023

J Thorac Dis

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“…For example, circ_0072083 has been shown to promote LUAD cell proliferation, migration, and invasion by modulating FGB expression. Similarly, circ_0067741 has been shown to inhibit LUAD cell proliferation and invasion by ordering the Hippo signaling pathway [ 30 ]. In this project, we revealed that circ_16601 activated the Hippo pathway by increasing FGB expression and ultimately contributed to LUAD progression.…”

Section: Introductionmentioning

confidence: 99%

Circ_16601 facilitates Hippo pathway signaling via the miR-5580-5p/FGB axis to promote my-CAF recruitment in the TME and LUAD progression

Zhou,

Li,

Zhao

et al. 2023

Respir Res

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Background Lung cancer represents a significant public health issue in China, given its high incidence and mortality rates. Circular RNAs (circRNAs) have been recently proposed to participate in the development and progression of tumors. Nevertheless, their particular roles in the pathogenesis of lung adenocarcinoma (LUAD), the tumor microenvironment (TME), and the underlying molecular mechanisms are still not well understood. Methods High-throughput sequencing was used to analyze the circRNAs expression profiles in 7 pairs of human LUAD tissues. shRNA was used to knockdown the YAP1 and FGB genes. RNA sequencing and RT-qPCR were performed to classify the regulatory effects of circ_16601 in LUAD cells. The progression effect of circ_16601 on lung cancer was investigated in vitro and in vivo. Results The circ_16601 is significantly elevated in LUAD tissues compared to adjacent normal lung tissues, and its high expression is positively associated with poor prognosis in LUAD patients. Additionally, circ_16601 overexpression promotes LUAD cell proliferation in vitro and increases xenograft tissue growth in mice in vivo; circ_16601 also could recruit fibroblasts to cancer associate fibroblasts. Mechanistically, circ_16601 can directly bind to miR-5580-5p, preventing its ability to degrade FGB mRNA and enhancing its stability. Subsequently, circ_16601 promotes the activation of the Hippo pathway in a YAP1-dependent manner, leading to LUAD progression. Conclusions Our findings shed valuable insights into the regulatory role of circ_16601 in LUAD progression and highlight its potential as a diagnostic and therapeutic target in LUAD. Overall, this study provides theoretical support to improve the prognosis and quality of life of patients suffering from this devastating disease.

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Circular RNAs-mediated angiogenesis in human cancers

et al. 2023

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Circular RNA circ_0067741 regulates the Hippo/YAP pathway to suppress lung adenocarcinoma progression by targeting microRNA-183-5p

Cited by 6 publications

References 28 publications

miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4

miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4

Circ_16601 facilitates Hippo pathway signaling via the miR-5580-5p/FGB axis to promote my-CAF recruitment in the TME and LUAD progression

Circular RNAs-mediated angiogenesis in human cancers

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