LncRNA CamK-A Regulates Ca2+-Signaling-Mediated Tumor Microenvironment Remodeling

Sang, Lingjie; Ju, Huai-Qiang; Liu, Guang-ping; Tian, Tian; Ma, Guolin; Lu, Yong; Liu, Zexian; Pan, Ruolang; Li, Ruihua; Piao, Hulin; Marks, Jeffrey R.; Yang, Luo-jia; Yan, Qingfeng; Wang, Wenqi; Shao, Jian‐Zhong; Zhou, Youhe; Zhou, Tian; Lin, Aifu

doi:10.1016/j.molcel.2018.10.024

Cited by 62 publications

(60 citation statements)

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“…Human carcinogenesis predominantly involves a disordered balance of cell proliferation, differentiation and apoptosis. A number of studies have provided evidence supporting that altered Ca [2]+ signaling contributes to tumorigenesis and tumor progression [23,24]. STIM1, the Ca [2]+ storage sensor protein with a single transmembrane domain localized to the ER, is the key component of SOCE.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

Zeng

et al. 2019

Bioengineered

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Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of cancer progression and its clinical relevance. The data demonstrated that the expression of the STIM1 was significantly higher in non-small-cell lung cancer (NSCLC) tissues than in benign lesions and was associated with advanced NSCLC T stage. Knockdown of STIM1 expression in NSCLC cell lines A549 and SK-MES-1 significantly inhibited cell proliferation and induces A549 and SK-MES-1 cell arrest at the G2/M and S phases of the cell cycle. Western blotting showed that the expression of cyclin-dependent kinase (CDK) 1 and CDK2 were reduced while knockdown of STIM1 expression. Furthermore, knockdown of STIM1 in NSCLC cells significantly reduced the levels of xenograft tumor growth in nude mice. These data indicate that aberrant expression of the STIM1 protein may contribute to NSCLC progression. Future studies should focus on targeting STIM1 as a novel strategy for NSCLC therapy.

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Section: Discussionmentioning

confidence: 99%

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

Zeng

et al. 2019

Bioengineered

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“…LncRNAs are emerging as important regulatory molecules of gene expression and have been functionally implicated in the regulation of multiple cellular processes as RNA molecules. The dysregulation of lncRNAs contributes to various cancer hallmarks [16][17][18] . However, until now, no lncRNA has been reported to participate in the installation, removal, or recognition of m 6 A on RNAs.…”

Section: Resultsmentioning

confidence: 99%

“…LncRNAs have been identified as significant factors in cells by regulating gene transcription (in cis or trans), chromatin remodeling, and mRNA splicing; producing endogenous small interfering RNAs (siRNAs) and microRNA precursors; changing protein localization; regulating protein activity; and organizing protein components 14,15 . The dysregulation of lncRNAs has been linked to the hallmarks of cancers and cancer patient survival time [16][17][18] . However, whether lncRNAs are involved in regulating the installation, removal or recognition of m 6 A on RNAs remains unexplored.…”

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confidence: 99%

An oncopeptide regulates m6A recognition by the m6A reader IGF2BP1 and tumorigenesis

et al. 2020

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N 6-methyladenosine (m 6 A) is the most prevalent modification in eukaryotic RNAs. The biological importance of m 6 A relies on m 6 A readers, which control mRNA fate and function. However, it remains unexplored whether additional regulatory subunits of m 6 A readers are involved in the m 6 A recognition on RNAs. Here we discover that the long noncoding RNA (lncRNA) LINC00266-1 encodes a 71-amino acid peptide. The peptide mainly interacts with the RNA-binding proteins, including the m 6 A reader IGF2BP1, and is thus named "RNAbinding regulatory peptide" (RBRP). RBRP binds to IGF2BP1 and strengthens m 6 A recognition by IGF2BP1 on RNAs, such as c-Myc mRNA, to increase the mRNA stability and expression of c-Myc, thereby promoting tumorigenesis. Cancer patients with RBRP high have a poor prognosis. Thus, the oncopeptide RBRP encoded by LINC00266-1 is a regulatory subunit of m 6 A readers and strengthens m 6 A recognition on the target RNAs by the m 6 A reader to exert its oncogenic functions.

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“…The mechanism has been uncovered that TUC339 could regulate the macrophage polarization, functioning as promotion of anti-inflammatory cytokines and angiogenesis, thereby accelerating tumor proliferation [41]. Sang et al showed that lncRNA CamK-A was involved in macrophage infiltration and angiogenesis by triggering the transcription of the NF-κB signaling pathway in tumor cells [80]. By promoting NF-κB downstream cytokines (e.g., VEGF, IL-6, and TNF-α), Camk-A could remodel tumor microenvironment to recruit macrophages to tumors and contribute to angiogenesis [80].…”

Section: Journal Of Immunology Researchmentioning

confidence: 99%

“…Sang et al showed that lncRNA CamK-A was involved in macrophage infiltration and angiogenesis by triggering the transcription of the NF-κB signaling pathway in tumor cells [80]. By promoting NF-κB downstream cytokines (e.g., VEGF, IL-6, and TNF-α), Camk-A could remodel tumor microenvironment to recruit macrophages to tumors and contribute to angiogenesis [80]. LncRNA LNMAT1 upregulated CCL2 and recruited M2 macrophages to the tumor, and promoted lymphatic metastasis via excretion of VEGF-C [81].…”

Section: Journal Of Immunology Researchmentioning

confidence: 99%

Involvement of lncRNAs and Macrophages: Potential Regulatory Link to Angiogenesis

Jia

Zhou

2020

Journal of Immunology Research

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Macrophages are involved in angiogenesis, an essential process for organ growth and tissue repair, and could contribute to the pathogenesis of angiogenesis-related diseases such as malignant tumors and diabetic retinopathy. Recently, long noncoding RNAs (lncRNAs) have been proved to be important in cell differentiation, organismal development, and various diseases of pathological angiogenesis. Moreover, it has been indicated that numerous lncRNAs exhibit different functions in macrophage infiltration and polarization and regulate the secretion of inflammatory cytokines released by macrophages. Therefore, the focus of macrophage-related lncRNAs could be considered to be a potential method in therapeutic targeting angiogenesis-related diseases. This review mainly summarizes the roles played by lncRNAs which associated with macrophages in angiogenesis. The possible mechanisms of the regulatory link between lncRNAs and macrophages in various angiogenesis-related diseases were also discussed.

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LncRNA CamK-A Regulates Ca2+-Signaling-Mediated Tumor Microenvironment Remodeling

Cited by 62 publications

References 0 publications

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

An oncopeptide regulates m6A recognition by the m6A reader IGF2BP1 and tumorigenesis

Involvement of lncRNAs and Macrophages: Potential Regulatory Link to Angiogenesis

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