MALAT1 promotes angiogenesis of breast cancer

Huang, Xiaojuan; Xia, Yu; He, Guifang; Zheng, Lulu; Cai, Yongping; Yin, Yuan; Wu, Qiang

doi:10.3892/or.2018.6705

Cited by 45 publications

(42 citation statements)

References 32 publications

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“…Each monomer contains two helix-loop-helix EF-hand-type motifs to bind Ca 2 + . [3][4][5][6][7][8] Therefore, atomic level in-depth characterization of the interaction between S100A4 andi ts target proteins is essential. It has gained increasinga ttention over recent decades because of its metastasis-promoting properties, as well as its role in the pathogenesis of rheumatoid arthritis and in fibrotic diseases.…”

mentioning

confidence: 99%

Multilevel Changes in Protein Dynamics upon Complex Formation of the Calcium‐Loaded S100A4 with a Nonmuscle Myosin IIA Tail Fragment

et al. 2016

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Dysregulation of Ca -binding S100 proteins plays important role in various diseases. The asymmetric complex of Ca -bound S100A4 with nonmuscle myosin IIA has high stability and highly increased Ca affinity. Here we investigated the possible causes of this allosteric effect by NMR spectroscopy. Chemical shift-based secondary-structure analysis did not show substantial changes for the complex. Backbone dynamics revealed slow-timescale local motions in the H1 helices of homodimeric S100A4; these were less pronounced in the complex form and might be accompanied by an increase in dimer stability. Different mobilities in the Ca -coordinating EF-hand sites indicate that they communicate by an allosteric mechanism operating through changes in protein dynamics; this must be responsible for the elevated Ca affinity. These multilevel changes in protein dynamics as conformational adaptation allow S100A4 fine-tuning of its protein-protein interactions inside the cell during Ca signaling.

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confidence: 99%

Multilevel Changes in Protein Dynamics upon Complex Formation of the Calcium‐Loaded S100A4 with a Nonmuscle Myosin IIA Tail Fragment

et al. 2016

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“…The long non-coding RNA MALAT1 has been demonstrated to regulate diverse cancer processes, including chemo-and radio-sensitivities (11,12). As a potential oncogenic lncRNA, MALAT1 was known to be upregulated in multiple cancers (13)(14)(15). This study reports the upregulation of MALAT1 in GC tissues and cells.…”

Section: Discussionmentioning

confidence: 81%

“…The MALAT1 is one of human tumor-related lncRNA that promotes the growth and metastasis of multiple cancers (11,12). Previous studies have demonstrated MALAT1 was frequently upregulated in human cancers by functioning as a potential oncogenic regulator in multiple cancers (13)(14)(15). However, the molecular targets of MALAT1 and detailed mechanisms are unclear.…”

mentioning

confidence: 99%

Targeting the MALAT1-miR-206-GLS axis enhances the apoptotic effects of gastric cancer cells by mild hyperthermia treatments

Shi

Jiao

et al. 2020

Preprint

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Background: To explore the molecular mechanisms and modulatory effects of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in the hyperthermia-induced gastric cancer cell death. Methods: Combined qRT-PCR and GLS activity detection of glutamine metabolism, we demonstrate the difference of expression of MALAT1 and miR-206 in normal or cancer tissue/ several cell lines and the roles of two in regulation of glutamine, respectively. The relation of MALAT1 and miR-206 was research by bioinformatical analysis and luciferase report. In addition, the molecular regulation between apoptotic effects and MALAT1-miR-206-GLS axis in gastric cancer after mild hyperthermia treatments were discovered by western blotting, luciferase report, quantitative real-time PCR (qRT-PCR), GLS activity detection of glutamine metabolism and cell viability test. Results: MALAT1 positively associated with GC by promoting glutamine metabolism under short time hyperthermia treatment, it involved in an adaptive reaction, an increased glutamine metabolism rate which could be further overridden by long time hyperthermia exposures. miR-206 could inhibit glutamine metabolism of GC and target 3’UTR of GLS which has oncogenic functions in GC directly. In addition, miR-206-suppresed glutamine metabolism was through direct targeting GLS. LncRNA MALAT1 inhibited miR-206 expression in GC by sponging it as a competing endogenous RNA. In summary, MALAT1-promoted glutamine metabolism was through the miR-206-GLS axis. Furthermore, we demonstrated effective approaches from the MALAT1-miR-206 axis for enhancing the mild hyperthermia-induced cancer death under a short time. Conclusions: Taken together, the MALAT1-miR-206-glutamine metabolism axis is a new strategy for enhancing the selectivity of hyperthermia treatments specific to GC cells

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“…In the TNBC mouse model, direct intravenous injection of ASRPS reduced angiogenesis and tumor growth. Only a few studies have identified lncRNAs regulating angiogenesis in BC (Huang et al, 2018b; Zhang et al, 2017a), and no studies have investigated angiogenesis-regulating polypeptide encoded by lncRNA in BC. Our data suggested that ASRPS is a potent antitumor peptide through down-regulating tumor angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

LncRNA-encoded polypeptide ASRPS inhibits triple-negative breast cancer angiogenesis

Wang

Zhu

et al. 2019

Journal of Experimental Medicine

163

101

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Triple-negative breast cancer (TNBC) is a subtype of breast cancer (BC) with the most aggressive phenotype and poor overall survival. Using bioinformatics tools, we identified LINC00908 encoding a 60–aa polypeptide and differentially expressed in TNBC tissues. We named this endogenously expressed polypeptide ASRPS (a small regulatory peptide of STAT3). ASRPS expression was down-regulated in TNBCs and associated with poor overall survival. We showed that LINC00908 was directly regulated by ERα, which was responsible for the differential down-regulation of LINC00908 in TNBCs. ASRPS directly bound to STAT3 through the coiled coil domain (CCD) and down-regulated STAT3 phosphorylation, which led to reduced expression of VEGF. In human endothelial cells, a mouse xenograft breast cancer model, and a mouse spontaneous BC model, ASRPS expression reduced angiogenesis. In a mouse xenograft breast cancer model, down-regulation of ASRPS promoted tumor growth, and ASRPS acted as an antitumor peptide. We presented strong evidence that LINC00908-encoded polypeptide ASRPS represented a TNBC-specific target for treatment.

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MALAT1 promotes angiogenesis of breast cancer

Cited by 45 publications

References 32 publications

Multilevel Changes in Protein Dynamics upon Complex Formation of the Calcium‐Loaded S100A4 with a Nonmuscle Myosin IIA Tail Fragment

Multilevel Changes in Protein Dynamics upon Complex Formation of the Calcium‐Loaded S100A4 with a Nonmuscle Myosin IIA Tail Fragment

Targeting the MALAT1-miR-206-GLS axis enhances the apoptotic effects of gastric cancer cells by mild hyperthermia treatments

LncRNA-encoded polypeptide ASRPS inhibits triple-negative breast cancer angiogenesis

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