Resistin promotes tumor metastasis by down-regulation of miR-519d through the AMPK/p38 signaling pathway in human chondrosarcoma cells

Tsai, Chun‐Hao; Tsai, Henry J.; Huang, Ho Ning; Hung, Chih Hung; Hsu, Chin Jung; Fong, Yi Chin; Hsu, Hsiang‐Chen; Huang, Yuan; Tang, Chih Hsin

doi:10.18632/oncotarget.2724

Cited by 75 publications

(67 citation statements)

References 45 publications

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“…The invasion assay was performed using the same transwell plate except for coating Corning® Matrigel® Matrix (Corning, NY, USA) in the lower chamber. Selection of invasive prostate cancer cells (PC-3-I3 and DU145-I5) was performed by using transwell invasion assay as described previously [26]. Briefly, the transwell inserts were coated with Matrigel, prostate cancer cells were resuspended in 1% FBS containing media and seeded into the wells in the upper layer, with the lower layer supplied with 10% FBS containing media.…”

Section: Methodsmentioning

confidence: 99%

“…Cells were transfected with siRNAs according to manufacturers’ recommendations on standard procedure [26, 27]. The siRNAs (ON-TARGETplus SMARTpool) were purchased from GE Dharmacon (Lafayette, CO, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted from PCa cells using a TRIzol kit as described previously [26]. Briefly, the reverse transcription reaction was performed using the oligo (dT) primer.…”

Section: Methodsmentioning

confidence: 99%

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Thrombospondin-2 promotes prostate cancer bone metastasis by the up-regulation of matrix metalloproteinase-2 through down-regulating miR-376c expression

et al. 2017

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BackgroundThrombospondin-2 (TSP-2) is a secreted matricellular glycoprotein that is found to mediate cell-to-extracellular matrix attachment and participates in many physiological and pathological processes. The expression profile of TSP-2 on tumors is controversial, and it up-regulates in some cancers, whereas it down-regulates in others, suggesting that the functional role of TSP-2 on tumors is still uncertain.MethodsThe expression of TSP-2 on prostate cancer progression was determined in the tissue array by the immunohistochemistry. The molecular mechanism of TSP-2 on prostate cancer (PCa) metastasis was investigated through pharmaceutical inhibitors, siRNAs, and miRNAs analyses. The role of TSP-2 on PCa metastasis in vivo was verified through xenograft in vivo imaging system.ResultsBased on the gene expression omnibus database and immunohistochemistry, we found that TSP-2 increased with the progression of PCa, especially in metastatic PCa and is correlated with the matrix metalloproteinase-2 (MMP-2) expression. Additionally, through binding to CD36 and integrin ανβ3, TSP-2 increased cell migration and MMP-2 expression. With inhibition of p38, ERK, and JNK, the TSP-2-induced cell migration and MMP-2 expression were abolished, indicating that the TSP-2’s effect on PCa is MAPK dependent. Moreover, the microRNA-376c (miR-376c) was significantly decreased by the TSP-2 treatment. Furthermore, the TSP-2-induced MMP-2 expression and the subsequent cell motility were suppressed upon miR-376c mimic stimulation. On the other hand, the animal studies revealed that the bone metastasis was abolished when TSP-2 was stably knocked down in PCa cells.ConclusionsTaken together, our results indicate that TSP-2 enhances the migration of PCa cells by increasing MMP-2 expression through down-regulation of miR-376c expression. Therefore, TSP-2 may represent a promising new target for treating PCa.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-017-0390-6) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Thrombospondin-2 promotes prostate cancer bone metastasis by the up-regulation of matrix metalloproteinase-2 through down-regulating miR-376c expression

et al. 2017

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“…Similarly, the levels of miR-519d are reduced in breast cancer tissues and cell lines, while overexpression of miR-519d inhibits cell proliferation and invasion and induces apoptosis in breast cancer cells, probably through targeting signal transducer and activator of transcription 3 (STAT3) [39]. Lastly, transfection of miR-519d into chondrosarcoma cells diminished resistin-induced cell migration and directly silenced the expression of MMP-2 [40]. Taken together, while available information supports a role for miR-519d in the regulation of cell invasion, migration, and proliferation, the effect of miR-519d in this context is divergent, and seems to depend on the context of specific tissues and tumors.…”

Section: The Expression and Function Of Mir-519d In Non-placental Tismentioning

confidence: 99%

The function of miR-519d in cell migration, invasion, and proliferation suggests a role in early placentation

Xie

Sadovsky

2016

Placenta

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The processes of proliferation, migration, and invasion of extravillous trophoblasts are critical for placental implantation and early development, and directly influence pregnancy outcome. Dysregulation of these processes has been associated with placental dysfunction, implicated in clinical conditions such as preeclampsia and placental accreta. Among diverse microRNA (miRNA) species that are expressed in placental trophoblasts, members of the chromosome 19 miRNA cluster (C19MC) stand out in their nearly exclusive expression in the placenta. Recent research on the function of C19MC miRNAs in normal cell physiology and during tumorigenesis identified one C19MC member, miR-519d, as a regulator of cell migration, invasion, and interaction with the extracellular matrix. In this review, we focus on the function of miR-519d in placental trophoblasts, where miR-519d regulates cell migration and invasion, and its aberrant expression is associated with preeclampsia. In cancer, the function of miR-519d as an oncomiR or a tumor-suppressor is dependent upon the tumor type. Further research on the biological function and regulation of miR-519d may illuminate previously unknown mechanisms that control cell migration and invasion.

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“…They control gene expression by binding to the 3 -UTR of mRNA through complementary base pairing. Dysfunctions of miRNAs are frequently found in malignancies, including chondrosarcoma [19,20]. Increasing studies have focused on the role of miRNAs in cancer progression and metastasis, and they have been proposed as intervening in numerous functions of cancer cells, including survival, apoptosis, autophagy, migration, invasion, angiogenesis and lymphangiogenesis [21].…”

Section: Introductionmentioning

confidence: 99%

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

et al. 2016

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Chondrosarcoma is the second most frequently occurring type of bone malignancy characterized by distant metastatic propensity. Vascular endothelial growth factor-C (VEGF-C) is the major lymphangiogenic factor, and makes crucial contributions to tumour lymphangiogenesis and lymphatic metastasis. Adiponectin is a protein hormone secreted predominantly by differentiated adipocytes. In recent years, adiponectin has also been indicated as facilitating tumorigenesis, angiogenesis and metastasis. However, the effect of adiponectin on VEGF-C regulation and lymphangiogenesis in chondrosarcoma has remained largely a mystery. In the present study, we have shown a clinical correlation between adiponectin and VEGF-C, as well as tumour stage, in human chondrosarcoma tissues. We further demonstrated that adiponectin promoted VEGF-C expression and secretion in human chondrosarcoma cells. The conditioned medium from adiponectin-treated cells significantly induced tube formation and migration of human lymphatic endothelial cells. In addition, adiponectin knock down inhibited lymphangiogenesis in vitro and in vivo We also found that adiponectin-induced VEGF-C is mediated by the calmodulin-dependent protein kinase II (CaMKII), AMP-activated protein kinase (AMPK) and p38 signaling pathway. Furthermore, the expression of miR-27b was negatively regulated by adiponectin via the CaMKII, AMPK and p38 cascade. The present study is the first to describe the mechanism of adiponectin-promoted lymphangiogenesis by up-regulating VEGF-C expression in chondrosarcomas. Thus, adiponectin could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis.

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Resistin promotes tumor metastasis by down-regulation of miR-519d through the AMPK/p38 signaling pathway in human chondrosarcoma cells

Cited by 75 publications

References 45 publications

Thrombospondin-2 promotes prostate cancer bone metastasis by the up-regulation of matrix metalloproteinase-2 through down-regulating miR-376c expression

Thrombospondin-2 promotes prostate cancer bone metastasis by the up-regulation of matrix metalloproteinase-2 through down-regulating miR-376c expression

The function of miR-519d in cell migration, invasion, and proliferation suggests a role in early placentation

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

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