LINC00467 is up-regulated by TDG-mediated acetylation in non-small cell lung cancer and promotes tumor progression

Zhu, Yuxing; Li, Jingjing; Bo, Hao; He, Dong; Xiao, Mengqing; Xiang, Lei; Gong, Lian; Hu, Yi; Zhang, Yeyu; Cheng, Ying; Deng, Liping; Zhu, Rongrong; Ma, Yupo; Cao, Ke

doi:10.1038/s41388-020-01421-w

Cited by 33 publications

(32 citation statements)

References 24 publications

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“…LINC00467 expression is aberrantly upregulated in multiple tumor tissues and can enhance cell proliferation in neuroblastoma ( 15 ), lung cancer ( 16 ), and glioma cells ( 17 ). LINC00467 expression is closely associated with worse prognosis of these tumors.…”

Section: Discussionmentioning

confidence: 99%

“…A previous study revealed that LINC00467 promoted proliferation and invasion, inhibited apoptosis, and contributed to axitinib resistance in hepatocellular carcinoma through miR-509-3p/PDGFRA ( 18 ). Another study demonstrated that LINC00467 enhances the progression of non-small cell lung cancer through the AKT signaling cascade, and TDG-induced acetylation is the pivotal factor that modulates the expression of LINC00467 ( 16 ). Hence, to investigate the physiological effects of LINC00467, downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion.…”

Section: Discussionmentioning

confidence: 99%

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LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

et al. 2021

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BackgroundThe long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression.MethodsWe used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial–mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated via the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an in vivo nude mouse model of tumorigenesis.ResultsWe established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo.ConclusionsOur study reveals that LINC00467 promotes prostate cancer progression via M2 macrophage polarization and the miR-494-3p/STAT3 axis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

et al. 2021

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“…LINC00152 is a lncRNA downstream of YAP1 that competes with miR-632 and miR-185-3p as an endogenous RNA that regulates the expression of FSCN1 to promote malignant proliferation and metastasis of colorectal cancer cells [7]. Previously, we found that LINC00467 could bind to AZGP1 and promote its degradation, activating the Akt signaling pathway to promote non-small cell lung cancer progression [8]. However, lncRNAs in TGCT have only rarely been investigated.…”

Section: Introductionmentioning

confidence: 99%

Integrated analysis of high-throughput sequencing data reveals the key role of LINC00467 in the invasion and metastasis of testicular germ cell tumors

Zhu

Liu

et al. 2021

Cell Death Discov.

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Long noncoding RNAs (lncRNAs) are involved in various physiological and pathological processes. However, the role of lncRNAs in testicular germ cell tumor (TGCT) has been rarely reported. Our purpose is to comprehensively survey the expression and function of lncRNAs in TGCT. In this study, we used RNA sequencing to construct the lncRNA expression profiles of 13 TGCT tissues and 4 paraneoplastic tissues to explore the function of lncRNAs in TGCT. The bioinformatics analysis showed that many lncRNAs are differentially expressed in TGCT. GO and KEGG enrichment analyses revealed that the differentially expressed lncRNAs participated in various biological processes associated with tumorigenesis in cis and trans manners. Further, we found that the expression of LINC00467 was positively correlated with the poor prognosis and pathological grade of TGCT using WGCNA analysis and GEPIA database data mining. In vitro experiments revealed that LNC00467 could promote the migration and invasion of TGCT cells by regulating the expression of AKT3 and influencing total AKT phosphorylation. Further analysis of TCGA data revealed that the expression was negatively correlated with the infiltration of immune cells and the response to PD1 immunotherapy. In summary, this study is the first to construct the expression profile of lncRNAs in TGCT. It is also the first study to identify the metastasis-promoting role of LNC00467, which can be used as a potential predictor of TGCT prognosis and immunotherapeutic response to provide a clinical reference for the treatment and diagnosis of TGCT metastasis.

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“…LINC00467 has been reported to be transcriptionally induced by STAT1 in lung adenocarcinoma cells ( 41 ); additionally, LINC00467 was up-regulated by TDG-mediated acetylation in non-small cell lung cancer ( 42 ). We had also tried to investigate the mechanisms responsible for the upregulation of LINC00467 in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

“…However, how does LINC00467 increase the protein level of LIN28B with the interaction of each other, the specific mechanism involved remains to be further explored. LINC00467 has been reported to be transcriptionally induced by STAT1 in lung adenocarcinoma cells (41); additionally, LINC00467 was up-regulated by TDG-mediated acetylation in non-small cell lung cancer (42). We had also tried to investigate the mechanisms responsible for the upregulation of LINC00467 in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA LINC00467 Correlates to Poor Prognosis and Aggressiveness of Breast Cancer

et al. 2021

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Breast cancer remains the leading cause of female cancer-related mortalities worldwide. Long non-coding RNAs (LncRNAs) have been increasingly reported to play pivotal roles in tumorigenesis and cancer progression. Herein, we focused on LINC00467, which has never been studied in breast cancer. Silence of LINC00467 suppressed proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) of breast cancer cells in vitro, whereas forced expression of LINC00467 exhibited the opposite effects. Furthermore, we demonstrated overexpression of LINC00467 promoted tumor growth, while knockdown of LINC00467 inhibited pulmonary metastasis in vivo. Mechanistically, LINC00467 down-regulated miR-138-5p by acting as a miRNA “sponge”. Besides, LINC00467 also up-regulated the protein level of lin-28 homolog B (LIN28B) via a direct interaction. A higher expression level of LINC00467 was observed in breast cancer tissues as compared to the adjacent normal counterparts and elevated LINC00467 predicted poor overall survival. Our findings suggest LINC00467 promotes progression of breast cancer through interacting with miR-138-5p and LIN28B directly. LINC00467 may serve as a potential candidate for the diagnosis and treatment of breast cancer.

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LINC00467 is up-regulated by TDG-mediated acetylation in non-small cell lung cancer and promotes tumor progression

Cited by 33 publications

References 24 publications

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

Integrated analysis of high-throughput sequencing data reveals the key role of LINC00467 in the invasion and metastasis of testicular germ cell tumors

Long Non-Coding RNA LINC00467 Correlates to Poor Prognosis and Aggressiveness of Breast Cancer

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