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RP11?284F21.9 promotes lung carcinoma proliferation and invasion via the regulation of miR?627?3p/CCAR1.

ABSTRACT: Lung carcinoma is a prominent cause of mortality among patients with cancer. Previous studies have reported the vital role of long non?coding RNAs (lncRNAs) in the malignant progression of lung cancer. lncRNA RP11?284F21.9 was originally identified to be expressed in lung carcinoma, but its specific function remains unknown. Therefore, the present study aimed to elucidate the role of lncRNA RP11?284F21.9 in lung carcinoma progression. The expression of RP11?284F21.9 in lung cell lines and tissues was measured using reverse transcription?quantitative PCR. The endogenous expression of RP11?284F21.9 was silenced using RNA interference, and cell viabilities were measured with a Cell Counting Kit?8 assay. The invasion and apoptosis of cells were determined via Transwell assays and flow cytometry, respectively. The protein expression levels were measured by western blotting. An increased expression of RP11?284F21.9 was identified in both lung carcinoma tissues and cells. Knockdown of RP11?284F21.9 in lung carcinoma cells inhibited cell proliferation and invasion, but promoted cell apoptosis. The present study identified the existence of a direct interaction between RP11?284F21.9 and microRNA (miRNA/miR)?627?3p. Mechanistically, it was demonstrated that RP11?284F21.9 promoted the proliferation and invasiveness of lung carcinoma cells, in part, via the regulation of miR?627?3p. Furthermore, cell division cycle and apoptosis regulator 1 (CCAR1) was identified as a target gene of miR?627?3p. The in vivo tumor growth assay also demonstrated that the knockdown of RP11?284F21.9 suppressed tumor growth, upregulated miR?627?3p and downregulated CCAR1 in the xenograft model of nude mice. Thus, the present findings indicated the tumor promoting functions of RP11?284F21.9 in the progression of lung carcinoma, and provided a novel lncRNA/miRNA axis as a target for the management of lung cancer.

SUBMITTER: Li D

PROVIDER: S-EPMC7448446 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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RP11‑284F21.9 promotes lung carcinoma proliferation and invasion via the regulation of miR‑627‑3p/CCAR1.

Li Dan D Wang Li L Feng Jin J Shen Yan-Wei YW Liu Li-Na LN Wang Yuan Y

Oncology reports 20200812 4

Lung carcinoma is a prominent cause of mortality among patients with cancer. Previous studies have reported the vital role of long non‑coding RNAs (lncRNAs) in the malignant progression of lung cancer. lncRNA RP11‑284F21.9 was originally identified to be expressed in lung carcinoma, but its specific function remains unknown. Therefore, the present study aimed to elucidate the role of lncRNA RP11‑284F21.9 in lung carcinoma progression. The expression of RP11‑284F21.9 in lung cell lines and tissue ...[more]

PMID: 32945522

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Project description:BackgroundEVA1A (Eva-1 homolog A), a novel protein involved in autophagy and apoptosis, functions as a tumor suppressor in some human primary cancers, including hepatocellular carcinoma (HCC). While it is consistently downregulated in several cancers, its involvement in hepatocarcinogenesis is still largely unknown.MethodsWe first detected the expression of EVA1A in HCC tissues and cell lines using RT‒qPCR, immunohistochemistry and western blotting and detected the expression of miR-103a-3p by RT‒qPCR. Then, bioinformatics prediction, dual-luciferase reporter gene assays and western blotting were used to screen and identify the upstream microRNA of EVA1A. After manipulating the expression of miR-103a-3p or EVA1A, wound healing, invasion, proliferation, colony formation, apoptosis, autophagy, mitosis and mitochondrial function assays, including mitochondrial membrane potential, ROS and ATP production assays, were performed to investigate the functions of miR-103a-3p targeting EVA1A in HCC cells. Apoptosis-related proteins were assessed by RT‒qPCR (TP53) or western blotting (TP53, BAX, Bcl-2 and caspase-3). Autophagy level was evaluated by observing LC3 puncta and examining the protein levels of p62, Beclin1 and LC3-II/I.ResultsWe found that EVA1A expression was decreased while miR-103a-3p expression was increased in HCC tissues and cell lines and that their expression was inversely correlated in HCC patients. The expression of miR-103a-3p was associated with HCC tumor stage and poor prognosis. miR-103a-3p could target EVA1A through direct binding to its 3'-UTR and suppress its expression. Overexpression of miR-103a-3p significantly downregulated the expression of EVA1A, TP53 and BAX, upregulated the JAK2/STAT3 pathway and promoted HCC cell migration, invasion and proliferation, while repression of miR-103a-3p dramatically upregulated the expression of EVA1A, TP53, BAX and cleaved-caspase-3, inhibited HCC cell migration, invasion and proliferation, and caused mitochondrial dysfunction and apoptosis. Overexpression of EVA1A significantly attenuated the cancer-promoting effects of miR-103a-3p in HCC cells, while knockdown of EVA1A alleviated the mitochondrial dysfunction and apoptosis caused by miR-103a-3p inhibition. Overexpression of EVA1A did not induce significant changes in autophagy levels, nor did it affect G2/M transition or mitosis.ConclusionThese findings indicate that the downregulation of the tumor suppressor EVA1A by miR-103a-3p potentially acts as a key mediator in HCC progression, mainly by inhibiting apoptosis and promoting metastasis. The miR-103a/EVA1A/TP53 axis provides a new potential diagnostic and therapeutic target for HCC treatment.

Dataset Information

RP11?284F21.9 promotes lung carcinoma proliferation and invasion via the regulation of miR?627?3p/CCAR1.

Publications

RP11‑284F21.9 promotes lung carcinoma proliferation and invasion via the regulation of miR‑627‑3p/CCAR1.

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