LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA

Zhen, Hongtao; Du, Peng; Yi, Qiang; Tang, Xiaolong; Wang, Tongqing

doi:10.1186/s12885-021-08882-6

Cited by 19 publications

(11 citation statements)

References 60 publications

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“…Our clinical examination results showed upregulated LINC00958 and underexpressed miR-625-5p in BC patients, indicating an inverse connection between the two genes in BC. This is consistent with the results of our previous research and related studies [ 23 , 24 ], confirming that LINC00958 is involved in the occurrence and development of BC and that its mechanism of action may be bound up with miR-625-5p. In the subsequent analysis of the relationship between them and clinical pathology of BC patients, the two genes were found to have a close connection with MI, LNM, DM, and histological grade of BC, which once again verifies our view.…”

Section: Discussionsupporting

confidence: 93%

LINC00958 Inhibits Autophagy of Bladder Cancer Cells via Sponge Adsorption of miR-625-5p to Promote Tumor Angiogenesis and Oxidative Stress

Xiao

Wang

Cheng

et al. 2022

Oxidative Medicine and Cellular Longevity

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Objective. This study further explored LINC00958’s role in promoting tumor angiogenesis (AG) and oxidative stress (OS) development by inhibiting BC cell autophagy through sponge adsorption of miR-625-5p. Methods. BC patients and healthy controls who visited our hospital between June 2017 and February 2019 were selected as the research group (RG) and the control group (CG), respectively, with a total of 133 study subjects. Peripheral blood LINC00958 and miR-625-5p in both cohorts of participants were detected. Additionally, human bladder transitional cell carcinoma cells (T24 and J82) and human normal urothelial cells (SV-HUC-1) were purchased. Alterations in cell biological behavior were observed after transfecting miR-625-5p-mimics, miR-625-5p-inhibition, and miR-625-5p-NC sequences into these cells, respectively. Besides, ELISA was performed to quantify inflammatory factors (IFs), AG indicators, and OS indexes in cells. Subsequently, a double luciferase reporter (DLR) assay was performed to verify the targeting relationship between LINC00958 and miR-625-5p. Finally, BALB/c-nu nude mice were purchased, and T24 cells transfected with silenced LINC00958 and miR-625-5p expression sequences were used to establish subcutaneous tumors to observe tumor growth and pathological changes. Results. RG exhibited higher LINC00958 and lower miR-625-5p than CG. LINC00958 and miR-625-5p were strongly linked to myometrial invasion (MI), lymph node metastasis (LNM), distant metastasis (DM), and histology in BC patients, and the increase of LINC00958 and the decrease of miR-625-5p predicted an increased risk of prognostic death in such patients. After miR-625-5p inhibition, the capacity of BC cells to proliferate, invade, and migrate enhanced and the AG, inflammatory response, and OS injury increased, while the apoptosis rate and autophagy ability decreased. The DLR assay revealed inhibited LINC00958WT fluorescence activity by miR-625-5p-mimics, while the biological behavior of BC cells cotransfected with sh-LINC00958 and miR-625-5p-inhibition had no difference with the functions of sh-control and miR-625-5p-NC cotransfected cells. Finally, the nude mouse tumorigenesis experiment showed that the tumor mass, volume, and histopathological features of the sh-LINC00958 group were decreased compared with the sh-control group, while those of the miR-625-5p-inhibition group were increased versus miR-625-5p-NC. Conclusions. In BC, LINC00958 is highly expressed while miR-625-5p is underexpressed. LINC00958 can inhibit cell autophagy to enhance cell activity; promote OS, inflammation, and AG; and regulate tumor immunity by targeting miR-625-5p, thus participating in the development of BC.

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Section: Discussionsupporting

confidence: 93%

LINC00958 Inhibits Autophagy of Bladder Cancer Cells via Sponge Adsorption of miR-625-5p to Promote Tumor Angiogenesis and Oxidative Stress

Xiao

Wang

Cheng

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Up-regulation of AURKA was correlated with poor outcomes in HCC patients 39 . Functionally, it plays multiple roles in regulating cancer cell proliferation, apoptosis, metastasis, stemness and genomic instability 13,40,41 . In HCC, AURKA promotes cancer metastasis and cancer stem cell properties 42 .…”

Section: Discussionmentioning

confidence: 99%

METTL16 Mediated LncRNA TIALD m6A Modification contributes to hepatocellular carcinoma metastasis via inducing AURKA lysosomal degradation

Zhao

Wang

Zhong

et al. 2023

Preprint

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The N6-methyladenosine (m6A) RNA methyltransferase METTL16 is an emerging player in RNA modification landscape and responsible for the deposition of m6A in a few transcripts. AURKA (aurora kinase A) has been confirmed as an oncogene in cancer development including hepatocellular carcinoma (HCC). Nevertheless, it remains unclear whether METTL16 mediated m6A modification of lncRNAs can regulate AURKA activation in cancer progression. Here we aimed to investigate the functional links between lncRNAs and the m6A modification in AURKA signaling and HCC progression. Here we show that LncRNA TIALD (transcript that induced AURKA Lysosomal degradation) was down-regulated in HCC tissues by METTL16 mediated m6A methylation to facilitate its RNA degradation, and correlates with poor prognosis. Functional assays reveal that TIALD inhibits HCC metastasis both in vitro and in vivo. Mechanistically, TIALD directly interacts with AURKA and facilitate its degradation through the lysosomal pathway to inhibited EMT and metastasis of HCC. AURKA’s specific inhibitor alisertib exerts effective therapeutic effect on liver cancer with low TIALD expression, which mightprovide a new insight into HCC therapy. Our study uncovers a negative functional loop of METTL16-TIALD-AURKA axis, and identifies a new mechanism for METTL16 mediated m6A-induced decay of TIALD on AURKA signaling in HCC progression, which may provide potential prognostic and therapeutic targets for HCC.

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“…Applying lncRNAs as biomarkers or intervention targets could provide new insights into predicting prognosis, survival and treatment outcome [31,32]. Many studies have shown that lncRNAs play an important role in BCa, and these experimental researches suggested that lncRNAs were associated with the proliferation and invasion of bladder cancer, indicating that they may serve as potential biomarkers for targeted therapy in bladder cancer [20][21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

“…LncRNAs are emerging regulators involved in gene expression and various physiological and pathological processes. Some scholars believe that abnormal lncRNAs in bladder cancer are closely related to the development and prognosis of the disease, and increasing evidence shows that lncRNAs have the potential to regulate ferroptosis, apoptosis and autophagy in bladder cancer, and play a complex and precise regulatory role in cancer initiation [20][21][22][23][24]. They not only regulate the proliferation, differentiation, invasion and metastasis of cancer cells but also regulate the metabolic reprogramming of cancer cells [25].…”

Section: Introductionmentioning

confidence: 99%

Identification and validation of a novel cuproptosis-related lncRNA gene signature to predict prognosis and immune response in bladder cancer

Chen

Guan

et al. 2022

Discov Onc

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Purpose Bladder cancer (BCa) is one of the most common malignant tumors in the urogenital system, characterized by the high recurrence rate, mortality rate and poor prognosis. Based on cuproptosis-related long noncoding RNAs (CRLs), this study set out to create a prediction signature to evaluate the prognosis of patients with BCa. Methods RNA-seq data including CRLs and related clinicopathological data were gathered from The Cancer Genome Atlas (TCGA) database (n = 428). The predictive signature was constructed after correlation analysis. Subsequently, relying on the analyzed data from the TCGA database and our sample collection, we examined and verified the connections between CRLs model and important indexes included prognosis, route and functional enrichment, tumor immune evasion, tumor mutation, and treatment sensitivity. Results Patients in the high-risk group had lower overall survival (OS) than that of low-risk group. Compared with clinicopathological variables, CRLs features have better predictive value according to receiver operating characteristic (ROC) curve. The expression level of CRLs was highly associated with the tumor progress, tumor microenvironment and tumor immune escape. Additionally, we identified that the mutation of TP53, TTN, KMT2D and MUC16 gene were founded in patients with BCa. Lapatinib, pazopanib, saracatinib, gemcitabine, paclitaxel and palenolactone had good antitumor effects for BCa patients in the high-risk group (all P < 0.001). Conclusion This study revealed the effects of CRLs on BCa and further established CRLs model, which can be used in clinic for predicting prognosis, immunological response and treatment sensitivity inpatient with BCa.

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LINC00958 promotes bladder cancer carcinogenesis by targeting miR-490-3p and AURKA

Cited by 19 publications

References 60 publications

LINC00958 Inhibits Autophagy of Bladder Cancer Cells via Sponge Adsorption of miR-625-5p to Promote Tumor Angiogenesis and Oxidative Stress

LINC00958 Inhibits Autophagy of Bladder Cancer Cells via Sponge Adsorption of miR-625-5p to Promote Tumor Angiogenesis and Oxidative Stress

METTL16 Mediated LncRNA TIALD m6A Modification contributes to hepatocellular carcinoma metastasis via inducing AURKA lysosomal degradation

Identification and validation of a novel cuproptosis-related lncRNA gene signature to predict prognosis and immune response in bladder cancer

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