The N-terminal polypeptide derived from vMIP-II exerts its anti-tumor activity in human breast cancer by regulating lncRNA SPRY4-IT1

Wu, Haihua; Wang, Yueyue; Chen, Tiantian; Yu, Li; Wang, Haifeng; Zhang, Lingyu; Chen, Sulian; Wang, Wenrui; Yang, Qingling; Chen, Changjie

doi:10.1042/bsr20180411

Cited by 11 publications

(5 citation statements)

References 37 publications

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“…Recently, SKA2 was also identified to exert a function in tumorigenesis. Aberrant expression patterns of SKA2 have been reported in lung cancer (27)(28)(29), breast cancer (30)(31)(32), osteosarcoma (33,34) and kidney cancer (35). Nevertheless, the potential roles of SKA2 in GC are unknown.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of microRNA‑520a‑3p inhibits the proliferation, migration and invasion via spindle and kinetochore associated 2 in gastric cancer

Ren

Jiang

et al. 2019

Oncol Lett

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MicroRNAs (miR) serve important roles in the development and progression of tumors by targeting different genes. miR-520a-3p reported in lung and breast cancers as a tumor suppressor gene. However, the expression and functional significance of miR-520a-3p is not completely understood in gastric cancer (GC). In the present study, it was demonstrated that the expression levels of miR-520a-3p were significantly downregulated in GC tissues and cells using RT-qPCR. In addition, downregulated expression of miR-520a-3p was associated with the clinical stage of the tumor and invasion in patients with GC. Furthermore, overexpression of miR-520a-3p significantly inhibited cell proliferation, invasion and migration in SGC-7901 and MGC-803 GC cell lines using proliferation, wound healing and cell invasion assays. Spindle and kinetochore associated 2 (SKA2) was upregulated in GC cells using western blot analysis and a target gene of miR-520a-3p; miR-520a-3p mimics significantly reduced SKA2 expression. In addition, upregulation of SKA2 protein expression SKA2 reversed the miR-520a-3p-mediated inhibition of SGC-7901 cell proliferation, migration and invasion. In conclusion, miR-520a-3p functioned as a tumor suppressor gene by targeting SKA2 in GC cell lines, and may serve as a novel prognostic and potential therapeutic marker.

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Section: Discussionmentioning

confidence: 99%

Upregulation of microRNA‑520a‑3p inhibits the proliferation, migration and invasion via spindle and kinetochore associated 2 in gastric cancer

Ren

Jiang

et al. 2019

Oncol Lett

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“…SPRY4‐IT1 acted as a factor which promoted progression of hepatocellular carcinoma by interacting with HNRNPL and influencing TNF signaling pathway 25 ; in non‐small‐cell lung cancer, SPRY4‐IT1 was an effective biomarker regulated by EZH2 40 ; high expression of SPRY4‐IT1 in colorectal cancer predicted poor prognosis 41,42 ; PI3K/Akt signaling pathway was activated by SPRY4‐IT1 in testicular germ cell tumor, meanwhile, cell growth, migration, and invasion were significantly enhanced 43 . Additionally, some studies confirmed SPRY4‐IT1 acted as an oncogene in breast cancer which related to poor prognosis, 44–46 however, the underlying mechanism of SPRY4‐IT1 promoting breast cancer was still fuzzy.…”

Section: Discussionmentioning

confidence: 92%

“…high expression of SPRY4-IT1 in colorectal cancer predicted poor prognosis 41,42 ; PI3K/Akt signaling pathway was activated by SPRY4-IT1 in testicular germ cell tumor, meanwhile, cell growth, migration, and invasion were significantly enhanced. 43 Additionally, some studies confirmed SPRY4-IT1 acted as an oncogene in breast cancer which related to poor prognosis, [44][45][46] however, the underlying mechanism of SPRY4-IT1 promoting breast cancer was still fuzzy.…”

Section: Discussionmentioning

confidence: 99%

PDK1‐stabilized LncRNA SPRY4‐IT1 promotes breast cancer progression via activating NF‐κB signaling pathway

Zhang

Chen

Yuan

et al. 2023

Molecular Carcinogenesis

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Pyruvate dehydrogenase kinase 1 (PDK1) is a widely known glycolytic enzyme, and some evidence showed that PDK1 promoted breast cancer by multiple approaches. However, very few lncRNAs have been identified to be associated with PDK1 in breast cancer in previous research. In this study, we found that lncRNA sprouty4‐intron transcript 1 (SPRY4‐IT1) was regulated by PDK1 with correlation analysis, and PDK1 upregulated SPRY4‐IT1 remarkably in breast cancer cells, as PDK1 interacted with SPRY4‐IT1 in the nucleus and significantly enhanced the stability of SRPY4‐IT1. Furthermore, SPRY4‐IT1 was highly expressed in breast cancer, significantly promoted the proliferation and inhibited apoptosis of breast cancer cells. In terms of mechanism, SPRY4‐IT1 inhibited the transcription of NFKBIA and the expression of IκBα, thus promoting the formation of p50/p65 complex and activating NF‐κB signaling pathway, which facilitated survival of breast cancer cells. Therefore, our finding reveals that PDK1/SPRY4‐IT1/NFKBIA axis plays a crucial role that promoting tumor progression, and SPRY4‐IT1 knockdown incombined with PDK1 inhibitor is promising to be a new therapeutic strategy in breast cancer.

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“…Several studies have indicated that lncRNA SPRY4‐IT1 is associated with the progress of breast cancer. LncRNA SPRY4‐IT1 is highly expressed in breast cancer cells, and N‐terminal polypeptide derived from viral macrophage inflammatory protein Ⅱ (NT21MP) inhibits the biological functions of breast cancer cells through lncRNA SPRY4‐IT1 . Another study has reported that proliferation is significantly suppressed when SPRY4‐IT1 is knocked down in breast cancer cells by targeting ZNF703 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2

Song

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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SPRY4‐intronic transcript 1 has been found in several kinds of cancers, but the role of SPRY4‐IT1 in breast cancer stem cells has not been studied. We investigated whether SPRY4‐IT1 is involved in the promotion of breast cancer stem cells (BCSCs). We used qRT‐PCR to detect the expression of SPRY4‐IT1 in MCF‐7 cells and MCF‐7 cancer stem cells (MCF‐7 CSCs). The effects of SPRY4‐IT1 on the proliferation and renewal ability of breast cancer cells were investigated by in vitro and in vivo assays (ie in situ hybridization, colony formation assay, sphere formation assay, flow cytometry assay, western blotting, xenograft model and immunohistochemistry). The mechanism of SPPRY4‐IT1 as a ceRNA was studied by a dual‐luciferase reporter assay and bioinformatic analysis. In our study, SPRY4‐IT1 was up‐regulated in MCF‐7 CSCs compared with MCF‐7 cells, and high SPRY4‐IT1 expression was related to reduced breast cancer patient survival. Furthermore, SPRY4‐IT1 overexpression promoted breast cancer cell proliferation and stemness in vitro and in vivo. In addition, SPRY4‐IT1 knockdown suppressed BCSC renewal ability and stemness maintenance in vivo and in vitro. The dual‐luciferase reporter assays indicated that SPRY4‐IT1 as a sponge for miR‐6882‐3p repressed transcription factor 7‐like 2 (TCF7L2) expression. Taken together, these findings demonstrated that SPRY4‐IT1 promotes proliferation and stemness of breast cancer cells as well as renewal ability and stemness maintenance of BCSCs by increasing the expression of TCF7L2 through targeting miR‐6882‐3p.

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The N-terminal polypeptide derived from vMIP-II exerts its anti-tumor activity in human breast cancer by regulating lncRNA SPRY4-IT1

Cited by 11 publications

References 37 publications

Upregulation of microRNA‑520a‑3p inhibits the proliferation, migration and invasion via spindle and kinetochore associated 2 in gastric cancer

Upregulation of microRNA‑520a‑3p inhibits the proliferation, migration and invasion via spindle and kinetochore associated 2 in gastric cancer

PDK1‐stabilized LncRNA SPRY4‐IT1 promotes breast cancer progression via activating NF‐κB signaling pathway

LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2

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